Should I scan or should I scope?

This paper proposes a clinical points-based method that can be used by less experienced orthopaedic surgeons who are faced with the dilemma 'Should I scan or should I scope?' By considering the history, the age of the patient and the clinical findings one can expect diagnostic performance equivalent to magnetic resonance imaging. The cost of MRI services must be considered when selecting patients for this investigation. We have suggested a threshold for requesting an MRI scan depending on the relative costs.     

The effect of sleepiness on performance monitoring: I know what I am doing,but do I care?

The behavioral, cognitive, and psychophysiological effects of extended wakefulness are well known. As time awake increases, errors become more common and are often attributed to lapses in attention. Such lapses can be reflected in the error-related negativity (Ne/ERN), a negative electroencephalogram deflection occurring after errors and is thought to be related to error detection or response conflict. Following the Ne/ERN, a positive deflection (error positivity, Pe) is also observed and is thought to reflect further evaluation of the error. To elicit Ne/ERNs, the Eriksen Flanker Task was administered to 17 women (aged 19-45 years) at two levels of alertness (4 and 20 h awake). After extended wakefulness, participants reported being subjectively sleepier and performing worse, but showed no significant difference in subjective effort. Across alertness conditions, they reported a similar number of subjective errors which closely matched an objective analysis of the errors. The Ne/ERN was not significantly reduced by sleepiness in contrast to the Pe which was reduced. Behavioral slowing after errors was larger in the alert than in the sleepy condition. These results show that after 20 h of wakefulness, individuals are reacting to their errors. However, further evaluation of the error, and remediation of these errors may be impaired despite continued effort.     

IκB激酶的研究进展

ＩκＢ激酶是核因子－κＢ／Ｒｅｌ蛋白参与一系列基因表达调控过程中最为关键的激酶，ＩκＫ包括分子量８５ｋＤ的ＩκＫα和分子量为８７ｋＤ的ＩκＫβ；其多肽分为激酶区，亮氨酸拉链样结构和螺旋环状结构。正常情况下，ＩκＫ以ＩκＫα，ＩκＫβ和ＮＩＫ三聚体复合物形式存在，ＮＩＫ激活后可活化ＩＫＫ而使ＩκＢｓ磷酸化，其中ＩκＫβ吏ＩκＢαＳｅｒ３２／３６和ＩκＢβＳｅｒ１９／２３等效磷酸化，而ＩκＢαＳｅｒ３     

How do I manage nocardiosis?

BackgroundNocardiosis is a rare infection that is often difficult to treat and may be life-threatening. There is no consensus on its management.ObjectivesOur aim was to provide the current evidence for the diagnosis and management of individuals with nocardiosis, and to propose a management approach for this uncommon infection.SourcesWe systematically searched the medical literature on nocardiosis for studies published between 2010 and 2020 and describing ten or more individuals.ContentNocardiosis, a primarily opportunistic infection which may occur in immunocompetent persons, most commonly involves the lungs and frequently disseminates to other sites including the central nervous system. The reference standard for Nocardia species identification is molecular biology, and the preferred method for antibiotic susceptibility testing (AST) is broth microdilution. Monotherapy seems appropriate for patients with primary skin nocardiosis or non-severe pulmonary disease; we reserve a multidrug regimen for more severe infections. Species identification and AST results are often missing at initiation of antibiotics. Trimethoprim-sulfamethoxazole is the preferred agent for initial therapy, because Nocardia is very often susceptible to this agent, and because it has been the keystone of nocardiosis treatment for years. Linezolid, to which Nocardia is almost always susceptible, may be an alternative. When combination therapy is required, the repertoire of companion drugs includes third-generation cephalosporins, amikacin and imipenem. Therapeutic modifications should take into account clinical response to initial therapy and AST results. Treatment duration of 6 months is appropriate for most situations, but longer durations are preferred for disseminated nocardiosis and shorter durations are reasonable in low-risk situations. Secondary prophylaxis may be considered in selected individuals with permanent immunosuppression.ImplicationsWe hereby provide the clinician with an easy-to-use algorithm for the management of individuals with nocardiosis. We also illuminate gaps in evidence and suggest future research directions.     

Ligand-independent transforming growth factor-β type I receptor signalling mediates type I collagen-induced epithelial-mesenchymal transition

Evidence suggests epithelial-mesenchymal transition (EMT) as one potential source of fibroblasts in idiopathic pulmonary fibrosis. To assess the contribution of alveolar epithelial cell (AEC) EMT to fibroblast accumulation in vivo following lung injury and the influence of extracellular matrix on AEC phenotype in vitro, Nkx2.1-Cre;mT/mG mice were generated in which AECs permanently express green fluorescent protein (GFP). On days 17-21 following intratracheal bleomycin administration, ~4% of GFP-positive epithelial-derived cells expressed vimentin or α-smooth muscle actin (α-SMA). Primary AECs from Nkx2.1-Cre;mT/mG mice cultured on laminin-5 or fibronectin maintained an epithelial phenotype. In contrast, on type I collagen, cells of epithelial origin displayed nuclear localization of Smad3, acquired spindle-shaped morphology, expressed α-SMA and phospho-Smad3, consistent with activation of the transforming growth factor-β (TGFβ) signalling pathway and EMT. α-SMA induction and Smad3 nuclear localization were blocked by the TGFβ type I receptor (TβRI, otherwise known as Alk5) inhibitor SB431542, while AEC derived from Nkx2.1-Cre;Alk5(flox/KO) mice did not undergo EMT on collagen, consistent with a requirement for signalling via Alk5 in collagen-induced EMT. Inability of a pan-specific TGFβ neutralizing antibody to inhibit effects of collagen together with absence of active TGFβ in culture supernatants is consistent with TGFβ ligand-independent activation of Smad signalling. These results support the notion that AECs can acquire a mesenchymal phenotype following injury in vivo and implicate type I collagen as a key regulator of EMT in AECs through signalling via Alk5, likely in a TGFβ ligand-independent manner.     

'What if I live?'

Recent advances in AIDS treatment, including the development of protease inhibitors, may eventually make AIDS a chronic disease to be managed rather than an immediately life-threatening one. This causes some psychological trauma in patients who have made financial choices based on their belief that they would die soon, and now have insufficient resources to support themselves. Others have developed survivor mentalities, and have some ambivalence about their change in status.     

131I治疗甲亢性心脏病

目的观察甲状腺功能亢进症并发甲亢性心脏病的临床特点，探讨其发嫡相关因素及^131I的有效治疗方法。方法选择53例甲心患者观察^131I治疗前后的临床表现，甲状腺激素水平的变化及门诊随访情况。结果^131I治疗后多数患者3个月内甲亢治愈，甲亢心伴随甲亢好转而好转，治愈率为86．8％（46例）。结论甲亢心根本的治疗是病因治疗，对并发症进行对症治疗，早期采用。^131I根治是有效的病因治疗，对甲亢心更有临床意义。     

血清肌钙蛋白I测定的临床意义

肌钙蛋白I(Tmponin I,Tn I)具有三种不同的同型物,分别定位于骨骼肌快肌、慢肌及心肌中.心肌肌钙蛋白I(Cardiac troponin I,cTnI)氨基酸序列有别于快、慢骨骼肌钙蛋白I(sTn I),使其免疫特性亦有别于骨骼肌中的两种同型物,具有心肌特异性[1].当心肌细胞受到损伤时,可引起血清cTn I浓度的变化.本文采用美国拜尔公司化学发光免疫分析法对93例患者血清进行cTnI浓度的测定,现将结果报道如下.     

I型胶原基因启动子研究进展

I型胶原由 α1(I)链 (COL1A1)与 α2 (I)链 (COL1A2 )组成 ,人 COL1A1与 COL1A2基因的启动子都已鉴定并克隆。调节转录的核因子有 Sp1、NF- 1、AP- 1、CBF、NF- кB、C- myb、c- Krox、BFCOL1、Zf9、Sp3、Smads、TGP、Egr- 1、TWIST与 NP/ NMP4等。在 COL1A1和 /或 COL1A2基因启动子上已鉴定出 TGFβ、糖皮质激素、TNFα、IFNγ与视黄酸等的应答元件     

抗DESMOPLAKIN I单克隆抗体的制备

作者从水牛鼻表皮中分离桥粒,提取桥粒中的Desmoplakin I(DPI)。用DPI作免疫原,免疫BALB/C小鼠,建立了一株分泌抗DPI单抗的细胞AD-1。免疫组化染色证实,该单抗与上皮组织呈阳性反应,与非上皮性组织呈阴性反应。提示该单抗可作为区分上皮性肿瘤与非上皮性肿瘤的免疫组化探针。     

IGF—I的免疫调节作用

IGF－I在促进生长发育和物质代谢方面的作用已得到证实并进行了广泛研究，近年来发现IGF－I还具有一定的免疫调节作用。本文对IGF－I对各类免疫细胞的功能调节及其意义作一概述。     

人异质性胞核核糖核蛋白I(hnRNP I)原核表达及初步应用

目的:克隆人异质性胞核核糖核蛋白I(hnRNP I)基因并构建原核表达载体,用纯化的重组蛋白进行系统性硬化症(SSc)体外诊断应用研究.方法:从体外培养的HeLa细胞中提取总RNA,用逆转录-聚合酶链反应(RT-PCR)扩增hnRNP I基因,构建原核表达载体pET-30a-hnRNP I,在原核表达系统E.coli BL21(DE3)中表达重组蛋白.重组蛋白纯化后作为抗原对包括系统性硬化症(SSc)、系统性红斑狼疮(SLE)、干燥综合征(SS)、混合型结缔组织病(MCTD)、未分化型结缔组织病(UCTD)、类风湿性关节炎(RA)、正常对照(control)在内的血清相应抗体进行ELISA检测.结果:成功构建了原核表达载体pET-30a-hnRNP I,在IPTG诱导下在E.coli BL21(DE3)中高效表达相对分子质量(M_r)为59 600的重组hnRNP I蛋白,重组蛋白可以可溶蛋白和包涵体蛋白两种形式存在.hnRNP I蛋白抗体在SSc中阳性率(48.72%)明显高于其他各组(P<0.05).结论:利用构建的原核表达载体成功表达出hnRNP I蛋白,此重组蛋白可用于SSc的临床诊断检测. UCTD) 类风湿性关节炎(RA)、正常对照(control)在内的血清相应抗体进行ELISA检测.结果:成功构建了原核表达载体pET-30a-hnRNP I,在IPTG诱导下在E.coli BL21(DE3)中高效表达相对分子质量(Mr)为59 600的重组hnRNP I蛋白,重组蛋白可以可溶蛋白和包涵体蛋白两种形式存在.hnRNP I蛋白抗体在SSc中阳性率(48.72%)明显高于其他各组(P<0.05).结论:利用构建的原核表达载体成功表达出hnRNP I蛋白,此重组蛋白可用于SSc的临床诊断检测. UCTD) 类风湿性关节炎(RA)、正常对照(control)