English英语译成Chinese汉语: Guidelines for solubility of peptides
General field: 医学
Detailed field: 生物学（生物技术、生化、微生物） | |
原文文本 - English英语
Guidelines for solubility of peptides
Peptides shorter than 10-15 amino acids will normally be soluble in water or aqueous buffer, unless they contain a very high proportion of hydrophobic amino acids. In general it is recommended to test the solubility of a small quantity of the delivered peptide in an aqueous buffer, unless the peptide is strongly hydrophobic.
The content of hydrophilic (acidic and basic), neutral and hydrophobic amino acids are written on Page 2 in the Certificate of Analysis for your peptide.
In general longer peptides containing less than 40% hydrophobic amino acids and more than 25-30% hydrophilic amino acids (acidic and basic) will normally dissolve in aqueous solutions (please see page 2 in the certificate of Analysis for your peptide for the distribution between hydrophilic, neutral and hydrophobic amino acids). It is recommended to dissolve these peptides in pure water or a buffered solution like PBS buffer, TRIS buffer etc. If the peptide contains significantly more acidic than basic amino acids, and the peptide is soluble in aqueous buffer in order, it is recommended to dissolve the peptide in a slightly basic buffer in order to increase the solubility. If the peptide contains significantly more basic than acidic amino acids and the peptide is soluble in aqueous buffer it is recommended to dissolve the peptide in a slightly acidic buffer in order to increase the solubility.
Longer peptides containing 40-65% hydrophobic amino acids will typically only be partially soluble in aqueous solutions. It is recommended to dissolve these peptides in a small quantity of organic solvent like DMF, TFA, acetonitrile etc. DMSO can also be used (If the sequence does not contain C, W or M). Peptides with moderate hydrophobicity can eventually be dissolved in ethanol. After a peptide has been dissolved in a minimum volume of organic solvent, an aqueous buffer or water can be added dropwise to the solvent. Stop immediately if the solution starts to show turbidity, and if the turbidity exists after some minutes then add more organic solvent, until the solution is clear again.
| 翻译文本 - Chinese汉语
多肽产品溶解指南
除非肽段中含有大量的疏水性氨基酸残基，少于10-15个氨基酸残基的多肽通常可以直接溶于水或水性溶剂。一般而言，如果多肽的疏水性不是很强，建议先称取少量多肽进行水溶性试验。
多肽产品分析证书的第2页上显示有该多肽含有的亲水性（酸性或碱性）、中性和疏水性氨基酸残基的比率。
疏水基少于40%且亲水基多于20%的长链多肽往往可以用水性溶剂溶解（疏水、中性和亲水基的比率请参照产品分析证书的第2页）。建议将此类多肽用纯水或水性缓冲液（例如,PBS缓冲液、TRIS 缓冲液等）进行溶解。当可溶于水的多肽中含有的酸性基显著多于碱性基时，可采用弱碱性溶剂以提高该多肽的可溶性。反之，当可溶于水的多肽中含有的碱性基显著多于酸性基时，则建议采用弱酸性溶剂以提高其可溶性。
含有40-65%的疏水基的长链多肽通常只能部分溶解于水性溶剂。这些多肽可以用少量有机溶剂（如DMF、TFA、乙腈等）来溶解。 如果肽段中不含半胱氨酸、色氨酸或蛋氨酸，该多肽还可以用DMSO溶解。呈轻度疏水性的多肽通常可以溶于乙醇中。先用最少量的有机溶剂溶解多肽，然后再逐滴加入水或水性溶液。当溶液开始出现混浊时应立即停止加液。混浊现象如果在数分钟内没有消失，可以再加入有机溶剂直到液体变清为止。
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English英语译成Chinese汉语: Basics: Pathophysiology
Detailed field: 医疗：医疗服务 | |
原文文本 - English英语
Basics: Pathophysiology
In all forms of PA, aldosterone production is excessive to the body's requirements and relatively autonomous with regard to its normal chronic regulator, the renin-angiotensin II system. This results in excessive sodium re-absorption through amiloride-sensitive epithelial sodium channels within the distal nephron, leading to HTN and suppression of renin-angiotensin II. Urinary loss of potassium and hydrogen ions, exchanged for sodium at the distal nephron, may result in hypokalaemia and metabolic alkalosis if severe and prolonged enough. The exact causes of excessive, autonomous aldosterone production in aldosterone-producing adenoma and bilateral adrenal hyperplasia are unknown, but genetic factors related to adrenal cortical ellular growth regulation and/or steroid biosynthesis are likely to be involved.
In FH-I, the causative hybrid gene encodes a hybrid enzyme of unique structure that synthesises aldosterone but, unlike CYP11B2, is regulated by adrenocorticotrophic hormone (ACTH) and not by angiotensin II. Aldosterone production in FH-I is therefore regulated by ACTH rather than by angiotensin II, and can be suppressed and managed by administering small doses of glucocorticoids such as dexamethasone.
Mutations in KCNJ5 (which encodes an inwardly-rectifying potassium channel) lead to reduced potassium/sodium channel selectivity and sodium influx, predisposing to cell membrane depolarisation, increased calcium influx, increased expression of genes promoting aldosterone synthesis, and increased aldosterone production by adrenocortical cells. How these effects lead to adrenal cell proliferation and tumour development remains uncertain.
Although morbidity in PA mainly results from HTN, experimental and clinical evidence strongly suggests that aldosterone excess can bring about adverse cardiovascular sequelae (including remodelling and fibrosis) independently of its hypertensive effects. In animal studies, both aldosterone excess and a high salt intake appear to be necessary for induction of cardiac fibrosis, and coronary vasculitis has been observed to be an early manifestation. These effects were preventable by the administration of mineralocorticoid receptor antagonists. The doses of aldosterone used in experimental studies have been very large, and the results of these studies may, therefore, have limited applicability to clinical situations. Nevertheless, several groups have convincingly demonstrated abnormalities in cardiovascular morphology or function in patients with PA that appear to be out of proportion to the elevation in BP. These have included:
• Increased left ventricular mass index and reduced diastolic function, both of which markedly improved following specific treatment of PA
• Reduced myocardial perfusion at rest and during exercise
• Increased myocardial backscatter (an echo marker of myocardial fibrosis)
• Increased proteinuria (as evidence of renal glomerular damage)
• A greater incidence of cardiovascular events, which was reversed following specific surgical or medical treatment.
• Evidence of left ventricular remodelling was also reported in individuals with genetically proven FH-I who had biochemical evidence of aldosterone excess but had not yet developed HTN.
| 翻译文本 - Chinese汉语
基础知识：病理生理学
在各种形式的假性醛固酮增多症中，醛固酮的合成大于身体的需要。它的合成相对自主，不受其慢性调节因子—肾素-血管紧张素II系统—的影响。过多的醛固酮导致远端肾单位上皮细胞阿米洛利敏感钠通道的钠离子再吸收显著增加，进而促进原发性高血压的产生并抑制肾素-血管紧张素II系统。远端肾单位钾-钠和氢-钠交换的增加直接导致钾离子和氢离子从尿液的排出增加。病情严重或持久迁延的情况下可能会出现低钾血症和代谢性碱中毒。自主性醛固酮合成过多、醛固酮瘤及双侧肾上腺皮质增生症的确切原因不明。但一些遗传性因素—如肾上腺皮质细胞生长失调和/或类固醇生物合成失调—很可能参与其中。
家族性醛固酮增多症I型患者的杂合基因编码生成一种分子结构独特的杂合酶。由此酶催化生成的醛固酮与CYP11B2型不同，它受促肾上腺皮质激素（ACTH）的调节，不受血管紧张素II的调节。家族性醛固酮增多症I型患者的醛固酮合成也因此受ACTH的调节而不是受血管紧张素II的调节，并可通过小剂量糖皮质激素（如地塞米松）进行干预治疗。
编码内向整流钾离子通道的KCNJ5基因的突变导致钾/钠离子通道的选择性降低、钠离子内流增加、诱发细胞膜去极化、钙离子内流增加、醛固酮合成基因的表达增加以及肾上腺皮质细胞醛固酮合成的增加。但这些效应引发肾上腺细胞增殖和肿瘤的机制仍不明确。
假性醛固酮增多症的病症主要由原发性高血压引起，但是实验和临床证据充分表明醛固酮过多所导致的心血管不良后遗症（包括重塑和纤维化）与它的升压作用无关。动物研究表明醛固酮过量和高盐摄入似乎是心脏纤维化的两个必要条件。研究同时发现冠状动脉炎是心脏纤维化的早期表现之一。盐皮质激素受体拮抗剂治疗可以预防上述病理改变的发生。实验研究中所用的醛固酮剂量总是很大，因此，其研究结果在临床上的适用性可能有限。虽说如此，有些研究团体的结果清晰地表明假性醛固酮增多症患者的心血管形态和功能的改变与血压升高的状况似乎是不相称的。此类研究结果列举如下：
• 左心室质量指数增加和舒张功能降低，经过特异性假性醛固酮增多症治疗后两项指标均明显好转
• 静止或运动时的心肌灌注减少
• 心肌背向散射（心肌纤维化的回声标记）增加
• 蛋白尿增加（肾小球损害的标志）
• 心血管事件的发生率较高，经相关手术或药物治疗后可逆转
• 研究结果证明遗传学证实为家族性醛固酮增多症I型且生化检查显示有醛固酮过多但还没有发展成为原发性高血压的个体有左室重构现象
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English英语译成Chinese汉语: Medical training material
General field: 医学
Detailed field: 医疗（总称） | |
原文文本 - English英语
Overall: During training try and do the discussions and practice slides with the trainees. This will help them to begin to understand how to have a collaborative conversation using these tools. Things to practice would be changing closed questions into open questions, listening (reading) and then coming up with reflections, and pulling out affirmations from a negative response. Practicing these skills should be a big part of the training sessions. Have examples always ready to share with trainees. When it comes to motivational interviewing the best way to learn is to practice. Set the trainees up to be successful and to be successful it takes ongoing practice.
Simple vs Complex Reflections: Simple reflections are the repeating of a word or two that may keep a patient moving in the conversation. They usually add little meaning to what the patient is saying. Complex reflections add meaning or emphasis to what the patient has said, making a guess at the unspoken content or what might come next.
This type of conversation is an art that is learned – a coach actively decides what to reflect on and what to ignore, what to emphasize or de-emphasize and what word to use to capture meaning.
| 翻译文本 - Chinese汉语
总体建议：在培训过程中，要积极与学员进行讨论，共同就课件内容进行实践练习。 只有如此，才能使学员学会使用这些技巧，从而能够（与患者）展开合作性的对话。 建议从以下三个方面着手练习：１）将封闭式提问变为开放式提问；２）聆听过后给予反馈信息；３）从（患者的）消极反应中找出积极的地方予以肯定。 训练这些技巧是培训课程的重要组成部分。 建议手边常备几个例子，以便随时与学员分享。 对于动机访谈，最好的学习方法仍然是实践。 鼓励学员为成功而努力，并让他们意识到唯有不断实践才能铺就成功之路。
简略反馈与精密反馈： 简略反馈是指在（与患者的）对话中重复一两个词，从而达到使患者继续说下去的目的。通常而言，这种反馈对患者所说得的内容既无添加亦无补充。 精密反馈则需要对患者所说进行分析示意，辨其轻重，猜其所未言，度其所欲言。
此类谈话是一门可以习得的艺术—指导员要有意识地判断（患者）所谈内容中哪些适合予以反馈，哪些需要忽略，哪些需要强化，哪些词语需要重申其义。
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English英语译成Chinese汉语: Patient Case Report
Detailed field: 医疗：医疗服务 | |
原文文本 - English英语
The patient is a 68 y/o female with recently diagnosis presumed pancreatic cancer status post ablation of pancreas head mass. Patient presented with 1 month abdominal distension. Imaging showed pancreatic head mass that was FDG avid with surrounding adenopathy that was not FDG avid but possibly due to PET sensitivity. Imaging reports do not describe adjacent blood vessels (report states that “pancreas body was surrounded with superior mesenteric vein” but not sure if that means mass encircled vein or not). EUS sample reported as “few small groups of heterogenic glandular epithelial cells exist in the blood clot tissue, part of which in the form of mucous epithelium so mutinous tumor is related, whereas pancreatic carcinoma could not be excluded.” The patient was treated with gamma knife.
This consultation was based on the limited medical records received. No pathology slides nor radiograph images were reviewed by our staff pathologist or radiologist respectively.
In regard to confirmation of diagnosis, based on the information provided, it is hard to opine if this patient has pancreatic adenocarcinoma. The report appears to suggest the biopsy was inadequate/non diagnostic sample. The issue now is that the lesion on the pancreas has been treated with radiation and thus likely will be more difficult to get a diagnostic sample.
Without a firm diagnosis of pancreatic adenocarcinoma, it is difficult to make treatment recommendations. There are other pathologies in the pancreas that are malignant, including pancreatic neuroendocrine tumor, lymphoma, or metastases from another primary site.
| 翻译文本 - Chinese汉语
患者，女，68岁，近期诊断为假定胰腺癌状态伴胰头肿块切除术后。 患者腹胀1月余。 FDG－PET成像显示胰头肿块氟脱氧葡萄糖浓聚（FDG avid)，而周围肿大的淋巴结未显示氟脱氧葡萄糖浓聚。但此结果不排除与PET的敏感性相关。 影像学报告没有对相邻血管进行描述（报告指出，“整个胰体被肠系膜上静脉覆盖”，但环绕肿块的静脉是否为肠系膜上静脉尚不清楚）。 内镜超声引导下细针穿刺活检报告显示：“血凝块组织中可见少量异种腺上皮细胞簇，有些呈黏膜上皮细胞形态，提示粘液瘤的存在，但胰腺癌不除外。” 患者接受了伽玛刀治疗。
本次的会诊意见是在医疗记录有限的情况下达成的。 我们的病理科专家和放射科医师没有对患者的病理切片和X光片进行检查评阅。
基于所获得的信息，很难判断该患者是否患有胰腺癌，我们也因此无法给出确切诊断。 报告的结果显示活检标本取材不理想，即为非诊断标本。 目前的问题是胰腺病变区已被放射线辐射过了，很难再取到诊断标本。
既然胰腺癌无法确诊，我们也就很难给出治疗建议。 此外，胰腺上也可能发生其他类型的恶性肿瘤，像胰腺神经内分泌肿瘤，淋巴瘤，或原发于其他部位的转移瘤。
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