關於 pathological analysis ，我們在網路上蒐集到這些相關的討論、資訊與評價

#抗疫也抗癌 #癌症頭號殺手💪💪
　　
🔺除了新冠肺炎，也來關心 #肺腺癌 最新研究突破！🔺
　　
#非編碼基因PTTG3P #加速肺腺癌細胞生長
⭐肺癌是全球及臺灣癌症十大死因之首，肺腺癌患者逐年增加。中研院生醫所周玉山研究員、施柔合博士後研究員組成的研究團隊發現，肺腺癌組織裡的非編碼核糖核酸「PTTG3P」表現愈高，會 #加速癌細胞成長，在小鼠實驗中也證實會 #降低存活率。
　　
若將PTTG3P表現量減少一半，腫瘤生成速度明顯減緩，顯著提升小鼠存活率。
　　
#此發現有助於化療用藥參考
⭐團隊也首次發現，肺腺癌化療病人癌組織裡面的PTTG3P表現越高，對於臨床化療藥物(順鉑和紫杉醇)產生抗藥性，使得治療效果打折扣。
建議化療用藥前，可先檢視患者癌組織裡的PTTG3P表現量，有助於提高療效，延長病人生命。
　　　　
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#PTTG3P #垃圾基因 #肺腺癌細胞增生兇手　　
第一作者施柔合表示，在人體細胞的核糖核酸中， 僅1/3可以轉譯出蛋白質執行生物功能；絕大部分的核糖核酸無此功能，被稱為非編碼核糖核酸 (noncoding RNAs, ncRNAs)，過去被定義為「垃圾基因」。
　　
近幾年來，科學家發現ncRNAs在疾病惡化及生物細胞學中扮演重要角色。研究團隊藉由與基因共舞(co-expression)原理及生物資訊分析，建構基因共同表現網路，找到6個ncRNAs與肺腺癌存活率相關，以 #PTTG3P表現最為顯著。
　　
💡此方法對於如何有效率、有系統地找到與疾病相關的ncRNAs，提供一大助力。
　　　　
周玉山指出，過去研究已知，肺腺癌細胞增生與下游調控的BUB1B基因表現有關，本次發現的「PTTG3P」就像黑幫老大，唆使其他小弟一同犯罪：「PTTG3P」和轉錄因子「FOXM1」交互作用，活化「BUB1B」的基因表現，三者像是合組「#犯罪者聯盟」，成為 #支援肺腺癌腫瘤成長的共犯結構。😈😈😈
　　
────────────

Postdoctoral researcher Dr. Jou-Ho Shih, in Dr. Yuh-Shan Jou’s research team at the Institute of Biomedical Sciences of Academia Sinica, who got her ph.D. degree in Genome and Systems Biology program at National Taiwan University/Academia Sinica, provided the systematic analysis for studying the biological functions and their following mechanisms of prognostic ncRNAs in lung adenocarcinoma (LUAD).
　　
Six prognostic ncRNAs and their associated co-expression gene networks were identified for functional prediction as prognostic markers of LUAD. Among them, one prognostic ncRNA, pituitary tumor transforming gene 3 pseudogene (PTTG3P), is prioritized to explore its detailed pathological functions and mechanisms owing to its upregulation in LUAD consistently associated with poor prognosis in multiple cohorts of LUAD patients.

────────────

📌本研究已於108年12月19日刊登在《核酸研究》(Nucleic Acids Research)。論文全文:https://academic.oup.com/…/…/doi/10.1093/nar/gkz1149/5680706
　　
📌〈肺腺癌研究新突破！非編碼基因讓癌細胞長更快〉
https://www.sinica.edu.tw/ch/news/6492
　　
📌〈Integrated analysis for predicting prognosis and pathological mechanisms of noncoding RNAs in cancers: up-regulation of PTTG3P is associated with poor prognosis and chemoresistance in lung adenocarcinoma〉
https://www.sinica.edu.tw/en/news/6492

────────────
📌媒體報導
[自由時報] 中研院團隊 研究新發現》「垃圾基因」會加速肺腺癌增生
https://news.ltn.com.tw/news/life/paper/1353423

[中央廣播電台] 中研院發現肺腺癌中的致命基因 宛如犯罪者聯盟
https://www.rti.org.tw/news/view/id/2052326

[公共電視] 肺腺癌最新研究 找出癌細胞生長關鍵
https://www.youtube.com/watch?v=77QxJQCuEg8

#抗疫也抗癌 #癌症頭號殺手💪💪
　　
🔺除了新冠肺炎，也來關心 #肺腺癌 最新研究突破！🔺
　　
#非編碼基因PTTG3P #加速肺腺癌細胞生長
⭐肺癌是全球及臺灣癌症十大死因之首，肺腺癌患者逐年增加。中研院生醫所周玉山研究員、施柔合博士後研究員組成的研究團隊發現，肺腺癌組織裡的非編碼核糖核酸「PTTG3P」表現愈高，會 #加速癌細胞成長，在小鼠實驗中也證實會 #降低存活率。
　　
若將PTTG3P表現量減少一半，腫瘤生成速度明顯減緩，顯著提升小鼠存活率。
　　
#此發現有助於化療用藥參考
⭐團隊也首次發現，肺腺癌化療病人癌組織裡面的PTTG3P表現越高，對於臨床化療藥物(順鉑和紫杉醇)產生抗藥性，使得治療效果打折扣。
建議化療用藥前，可先檢視患者癌組織裡的PTTG3P表現量，有助於提高療效，延長病人生命。
　　　　
────────────
　　
#PTTG3P #垃圾基因 #肺腺癌細胞增生兇手　　
第一作者施柔合表示，在人體細胞的核糖核酸中， 僅1/3可以轉譯出蛋白質執行生物功能；絕大部分的核糖核酸無此功能，被稱為非編碼核糖核酸 (noncoding RNAs, ncRNAs)，過去被定義為「垃圾基因」。
　　
近幾年來，科學家發現ncRNAs在疾病惡化及生物細胞學中扮演重要角色。研究團隊藉由與基因共舞(co-expression)原理及生物資訊分析，建構基因共同表現網路，找到6個ncRNAs與肺腺癌存活率相關，以 #PTTG3P表現最為顯著。
　　
💡此方法對於如何有效率、有系統地找到與疾病相關的ncRNAs，提供一大助力。
　　　　
周玉山指出，過去研究已知，肺腺癌細胞增生與下游調控的BUB1B基因表現有關，本次發現的「PTTG3P」就像黑幫老大，唆使其他小弟一同犯罪：「PTTG3P」和轉錄因子「FOXM1」交互作用，活化「BUB1B」的基因表現，三者像是合組「#犯罪者聯盟」，成為 #支援肺腺癌腫瘤成長的共犯結構。😈😈😈
　　
────────────

Postdoctoral researcher Dr. Jou-Ho Shih, in Dr. Yuh-Shan Jou’s research team at the Institute of Biomedical Sciences of Academia Sinica, who got her ph.D. degree in Genome and Systems Biology program at National Taiwan University/Academia Sinica, provided the systematic analysis for studying the biological functions and their following mechanisms of prognostic ncRNAs in lung adenocarcinoma (LUAD).
　　
Six prognostic ncRNAs and their associated co-expression gene networks were identified for functional prediction as prognostic markers of LUAD. Among them, one prognostic ncRNA, pituitary tumor transforming gene 3 pseudogene (PTTG3P), is prioritized to explore its detailed pathological functions and mechanisms owing to its upregulation in LUAD consistently associated with poor prognosis in multiple cohorts of LUAD patients.

────────────

📌本研究已於108年12月19日刊登在《核酸研究》(Nucleic Acids Research)。論文全文:https://academic.oup.com/nar/advance-article/doi/10.1093/nar/gkz1149/5680706
　　
📌〈肺腺癌研究新突破！非編碼基因讓癌細胞長更快〉
https://www.sinica.edu.tw/ch/news/6492
　　
📌〈Integrated analysis for predicting prognosis and pathological mechanisms of noncoding RNAs in cancers: up-regulation of PTTG3P is associated with poor prognosis and chemoresistance in lung adenocarcinoma〉
https://www.sinica.edu.tw/en/news/6492

────────────
📌媒體報導
[自由時報] 中研院團隊 研究新發現》「垃圾基因」會加速肺腺癌增生
https://news.ltn.com.tw/news/life/paper/1353423

[中央廣播電台] 中研院發現肺腺癌中的致命基因 宛如犯罪者聯盟
https://www.rti.org.tw/news/view/id/2052326

[公共電視] 肺腺癌最新研究 找出癌細胞生長關鍵
https://www.youtube.com/watch?v=77QxJQCuEg8

Manipulating vital signs in septic shock: which one(s) and how?

The interplay between elevated body temperature and the outcome of critically ill patients is complex. While it is widely accepted—albeit with variable strength of the evidence—that control of fever in patients with neurological compromise is advantageous, in most other cohorts it is not clear. On one hand, control of fever reduces metabolic demand and its treatment may be beneficial. On the other hand, fever is an adaptive response to infection and its treatment may be deleterious.
In their previous study, Schortgen and colleagues randomized patients with septic shock to a regimen of either permissive fever or external cooling to a normothermia goal. They observed a significant positive effect not only on their primary outcome of reduced vasopressor use but also on overall mortality associated with temperature control (14-day mortality 19 % with cooling vs. 34 % in controls, p = 0.013). In the present study, they conducted a further secondary analysis in order to investigate the confounding effects of heart rate on mortality. This question was raised in part related to an open label clinical trial that showed a significant reduction in mortality among septic shock patients randomized to heart rate control (<95/min) by means of an esmolol infusion as compared to controls. In their present analysis, they observed that the effect of temperature control on mortality was not mediated by control of heart rate.
Based on these data, one may come to the conclusion that fever should be controlled in patients with septic shock. However, there are some key issues which must be taken into consideration.
While the results of the original study by Schortgen are compelling, treatment of fever in septic patients has been by no means conclusively demonstrated to be beneficial. Observational studies including hundreds of thousands of patients have documented highly variable results [5, 6]. In addition, the overall body of clinical trials to date investigating anti-pyretic therapy in critically ill neurologically intact patients has not shown any overall benefit. Finally, we have observed numerous examples of small studies demonstrating dramatic mortality reductions associated with a number of different interventions in septic shock that could not be replicated in subsequent larger definitive studies.
Another important consideration in evaluating the studies reported by Schortgen et al. is that the confounding effects of beta-blocker use on outcome, whether successful or not in heart rate control, is not clear. Similarly, the study by Morelli et al. did not report on specifics regarding temperature control. While the current study by Schortgen et al. supports that the effect of temperature control on outcome is independent of heart rate, we are left wondering what would have been the effect of temperature had beta-blockade been applied systematically? To adequately address this question, the development of a factorial randomized control trial is required.
Further, in a more general sense, it is key to distinguish whether vital signs such as temperature and heart rates are elevated or decreased as a beneficial compensatory mechanism, implying that they should be left alone, or that vitals represent exhausted or counterproductive values which require manipulation by critical care specialists (Fig. 1). This is highly complex given that the transition of a vital sign from compensating (physiological) to decompensating (or pathological) may depend on many simultaneously acting circumstances, such as the underlying disease, the cross-talk with other affected organs, and physiological reserve of the patient. Furthermore, these may vary both inter- and intra-individually over time. Examples of such transitions into decompensated vitals on which more consensus exists include malignant hyperthermia (i.e., cool the patient), stress cardiomyopathy (i.e., start inotropic drugs) but also hypotension in compensated heart failure in an outpatient situation versus hypotension in cardiac shock. With regard to the example of heart failure, it is obvious that the patient with a blood pressure of 80/50 mmHg with compensated heart failure requires no intervention, whereas progression to decompensated heart failure and subsequent shock in another patient with the same blood pressure requires immediate treatment. So, theoretically, trials that include both the physiologically compensated and decompensated subjects for interventions that modify specific vital signs (e.g., blood pressure) may wrongfully practise “one size fits all”, when in fact selection for such interventions based on specific patient characteristics—even with a remarkably similar underlying condition—is essential.

http://bit.ly/1ZDVTIF