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Objective: Mediastinal nodal metastasis is related to poor prognosis in surgically resected non-small-cell lung cancer (NSCLC) and the prognosis becomes worse with an increasing number of nodal stations involved. However, intra-operative designation of each nodal station might be difficult and confusing because of the adjacency of the nodal stations, and this may cause inaccurate nodal staging. The new concept of a 'nodal zone' was proposed by the IASLC lung cancer staging project (IALC, International Association for the Study of Lung Cancer), and we investigated the impact of the 'nodal zone' on the survival of pathological N2 patients. Methods: From a total of 1186 patients with NSCLC, who underwent surgical resection with curative intent, we analysed the survival data of 217 patients with ipsilateral mediastinal metastasis retrospectively. Results: The operative mortality rate was 1.4% (three patients) and median follow-up period was 35.4 months. The 5-year overall survival rate was 36.5% (median: 39.3 months; confidence interval (CI): 32.05-46.62). Median disease-free survival was 17.4 months (CI: 13.84-21.03). Overall and disease-free survival were better in the single-zone metastasis group than in the multiple zone group (median: 48.5 vs 33.4 months, p=0.001, CI: 32.05-46.62, and 20.4 vs 10.6 months, p<0.001, CI: 13.84-21.03). Among those of the single nodal zone metastasis group, no differences were found between the single and multiple nodal station metastasis groups in overall and disease-free survival. Conclusions: Patients with single nodal zone metastasis showed favourable outcomes compared with the multiple zone metastasis group. Even though two or more nodal stations were involved, the outcome was favourable if the nodal stations involved were confined to a single nodal zone. In conclusion, patients with single nodal zone metastasis can benefit from surgical resection.
<P>TWIK-related two-pore domain K+ channels (TREKs) are regulated by intracellular pH (pH(i)) and Phosphatidylinositol 4,5-bisphosphate (PI(4,5)P-2). Previously, Glu(306) in proximal C-terminal (pCt) of mouse TREK-1 was identified as the pH(i)-sensing residue. The direction of PI(4,5)P-2 sensitivity is controversial, and we have recently shown that TREKs are inhibited by intracellular ATP via endogenous PI(4,5)P-2 formation. Here we investigate the anionic and cationic residues of pCt for the pH(i) and ATP-sensitivity in human TREK-2 (hTREK-2). In inside-out patch clamp recordings (I-TREK-2,I-i-o), acidic pH(i)-induced activation was absent in E332A and was partly attenuated in E335A. Neutralization of cationic Lys (K330A) also eliminated the acidic pH(i) sensitivity of I-TREK-2,I-i-o. Unlike the inhibition of wild-type (WT) I-TREK-2,I-i-o by intracellular ATP, neither E332A nor K330A was sensitive to ATP. Nevertheless, exogenous PI(4,5)P-2 (10 mu M) abolished ITREK-2 i-o in all the above mutants as well as in WT, indicating unspecific inhibition by exogenous PI(4,5)P-2. In whole-cell recordings of TREK-2 (I-TREK-2,I-w-c), K330A and E332A showed higher or fully active basal activity, showing attenuated or insignificant activation by 2-APB, arachidonic acid, or acidic pH(e) 6.9. I-TREK-1,I-w-c of WT is largely suppressed by pH(e) 6.9, and the inhibition is slightly attenuated in K312A and E315A. The results show concerted roles of the oppositely charged Lys and Glu in pCt for the ATP-dependent low basal activity and pH(i) sensitivity.</P>
Sivanandhan, Ganeshan,Arunachalam, Chinnathambi,Vasudevan, Venkatachalam,Kapildev, Gnanajothi,Sulaiman, Ali Alharbi,Selvaraj, Natesan,Ganapathi, Andy,Lim, Yong Pyo Springer-Verlag 2016 Plant biotechnology reports Vol.10 No.2
Cho, Yuna,Kim, Hye Kwon,Lee, Kyunglee,Kim, Hyun Woo,Park, Kyum Joon,Sohn, Hawsun,Choi, Youngmin,Park, Sung-Kyun,Jeong, Dae Gwin,Kim, Ji Hyung Springer-Verlag 2018 Conservation genetics resources Vol.10 No.4
Ryu, Young-Kyoung,Park, Hye-Yeon,Go, Jun,Choi, Dong-Hee,Kim, Yong-Hoon,Hwang, Jung Hwan,Noh, Jung-Ran,Lee, Tae Geol,Lee, Chul-Ho,Kim, Kyoung-Shim Springer-Verlag 2018 Molecular Neurobiology Vol.55 No.7