医学英语研究论文

Genes, autoimmunity and pathogenesis of rheumatic heart diseaseL Guilherme1, KF Köhler1, E Postol1, J Kalil21 Heart Institute (InCor), School of Medicine, University of São Paulo, São Paulo;Institute for Immunology Investigation, National Institute for Science and Technology, University of São Paulo, São Paulo, Brazil2 Heart Institute (InCor), School of Medicine, University of São Paulo, São Paulo;Institute for Immunology Investigation, National Institute for Science and Technology, University of São Paulo, São Paulo;Clinical Immunology and Allergy Division, School of Medicine, University of São Paulo, São Paulo, BrazilClick here for correspondence address and emailAbstractPathogenesis of rheumatic heart disease (RHD) remains incompletely understood. Several genes associated with RHD have been described; most of these are involved with immune responses. Single nucleotide polymorphisms in a number of genes affect patients with RHD compared to controls. Molecular mimicry between streptococcal antigens and human proteins, including cardiac myosin epitopes, vimentin and other intracellular proteins is central to the pathogenesis of RHD. Autoreactive T cells migrate from the peripheral blood to the heart and proliferate in the valves in response to stimulation with specific cytokines. The types of cells involved in the inflammation as well as different cytokine profiles in these patients are being investigated. High TNF alpha, interferon gamma, and low IL4 are found in the rheumatic valve suggesting an imbalance between Th1 and Th2 cytokines and probably contributing to the progressive and permanent valve damage. Animal model of ARF in the Lewis rat may further contribute towards understanding the ARF.Keywords: Autoimmunity, rheumatic Heart disease, susceptibility genesHow to cite this URL:Guilherme L, Köhler KF, Postol E, Kalil J. Genes, autoimmunity and pathogenesis of rheumatic heart disease. Ann Pediatr Card [serial online] 2011 [cited 2012 Nov 2];4:13-21. Availablefrom: /text.asp?2011/4/1/13/79617Rheumatic heart disease (RHD) is still a major health problem in several countries due to the heart lesions that follow a rheumatic fever (RF) episode in 30-45% of patients. The incidence of acute RF (ARF) in some developing countries exceeds 50 per 100,000 children. The worldwide prevalence of RHD is at least 15.6 million cases, and this disease is responsible for around 233,000 deaths/year. [1] RHD results from autoimmune reactions triggered by an untreated S. pyogenes throat infection leading to severe valvular damage in genetically susceptible individuals. Recurrences of ARF play an important role in the worsening of valvularlesionss. [2],[3]In the present review, we focus on genetic susceptibility factors, their role in the development of RF and RHD, and the mechanisms that lead to autoimmune reactions and permanent valvular damage. Animal models of the disease will also be discussed, as will prospective vaccines for the prevention of RF and RHD.Innate and Adaptive Immune Responses : A Brief ReviewProtection against pathogens in the humans relies on complex interactions between innate and adaptive immunity. Most of the pathogens that enter the body are recognized initially by the innate immune system. [4]This defense mechanism is not antigen-specific and is instead focused on the recognition of a limited number of specific patterns that are shared by groups of pathogens (pathogen-associated molecular patterns - PAMPs) by pattern recognition receptors (PRRs) in the host. These PRRs can be soluble in human serum or cell-associated. [5],[6]The molecules that initiate the complement cascade are examples of soluble PRRs. The complement system is part of the innate immune system and consists of many proteins involved in a cascade of proteolysis and protein complex assembly that culminates in the elimination of invading pathogens. [6] Several components of the bacterial cell surface combine with PRRs such as Ficolin family of proteins, or Mannan binding lectins (MBL). These complexes, in turn combine with serine proteases and lead to complement activation via lectin pathway resulting in opsonophagocytosis of the invading pathogen, apoptosis, or modulation of inflammation. [7],[8],[9],[10]Toll-like receptors (TLRs) are pivotal cell-associated PRRs in the innate immune system. These receptors are capable of recognizing a wide spectrum of organisms, including viruses, bacteria and other parasites, and are classified into different groups based on their localization (cell surface or intracellular) and the type of PAMPs they recognize. TLR activation leads to the production of proinflammatory cytokines that enable macrophages and dendritic cells (DC) to eliminate invading pathogens. DCs can stimulate T cell expansion and differentiation, initiating an adaptive immune response. [4] The molecules produced during the innate immune response act as signals to activate adaptive immune responses. Antigen presenting cells (APCs), such as DCs, are activated and express costimulatory (CD80 and CD86) and MHC molecules on their cell surface that enable these cells to present processed antigens to T cells through the T cell receptor (TCR). Class I MHC molecules, such as HLA-A, -B and -C, present peptides derived from intracellular pathogens to CD8 + T cells, while class II MHC molecules, such as HLA-DR, -DQ and -DP, present peptides derived from extracellular pathogens to CD4 + T cells, which secrete a wide range of cytokines and have both effector and regulatory roles. Cytokines such as TNF-a and IFN-g act at the site of infection and can affect pathogensurvival and control the immune response. Activation of CD4 + T cells not only leads to the expansion of CD4 + effector cells, but also can promote the expansion and differentiation of antigen-specific CD8 + T cells and B cells. [4]CytokinesCytokines seem to play a pivotal role in the activation of immunological and inflammatory responses in RF. It has been shown that peripheral blood mononuclear cells (PBMC) from children with RF produce more TNF-α than heal thy controls. [20] Moreover, interleukin-6 (IL-6) and TNF-α are considered inducers of the acute phase of RF and are strongly correlated with C-reactive protein. [21],[22]TNF-α is a proinflammatory cytokine that has been associated with the severity of different autoimmune and inflammatory diseases. The gene that encodes this cytokine is located within the MHC region on chromosome 6p21.3. This region is highly polymorphic, and the TNF-alpha gene also contains a large number of polymorphisms. [23] Some of these were investigated in RF/RHD patients in different countries. An SNP in the promoter region of TNF-alpha (-308A) was associated with susceptibility to RHD in Mexico, Turkey, Brazil, and Egypt. [21],[22],[23],[24],[25],[26] The TNF-alpha -238G allele was also associated with RHD in Mexican and Brazilian patients. [24],[25] The TNF-alpha gene has a proinflammatory effect and is probably associated with the exacerbation of the inflammatory response in RF/RHD patients who present with high serum TNF-α levels[20],[22],[27],[28] and large numbers of TNF-α-producing cells in the throat and valves. [29]Polymorphisms in other cytokine genes have also been investigated and seem to be involved with the disease. These include TGF beta1, [30],[31] interleukin-1 receptor antagonist (IL1Ra), [32] interleukin 10, [21] amongst others. In Taiwanese RHD patients, both the -509T and 869T alleles of TGF beta 1 were found to be risk factors for the development of valvular RHD lesions. [30] Similar results were found in Egyptian patients. [31] RHD patients from Egypt and Brazil with severe carditis showed low frequencies of allele 1 for IL1Ra, suggesting the absence of control of the inflammatory process. [21],[32]Interleukin-10 (IL-10) is one of the most important anti-inflammatory cytokines, together with TGF-β and IL-35. It is produced by activated immune cells, especially monocytes/macrophages and T cell subsets, including regulatory T cells (Tr1 and Treg) and Th1 cells. IL-10 acts through a transmembrane receptor complex, and regulates the functions of many different immune cells. [33]The gene encoding human IL-10 is located on chromosome 1. A large number of polymorphisms have been identified in the IL-10 gene promoter. The genotype IL-10 -1082G/A that is overrepresented in RHD Egyptian patients is associated with the development of multiple valvular lesions (MVL) and with the severity of RHD. [21] More recently, polymorphism in cytotoxic T cell Lymphocyte antigen 4 (CTLA-4), which is a negative regulator of T cell proliferation has also been shown in Turkish RHD patients.[34]Human Leucocyte AntigenHuman leucocyte antigen (HLA) molecules are encoded by the HLA genes (-A, -B, -C, -DR, -DQ and -DP), which are located on the short arm of human chromosome 6. Early studies of susceptibility for RF/RHD pointed out the association of the disease with several HLA class II alleles, mainly those encoded by the DR and DQ genes.Several HLA class II alleles were described in locations around the world [Figure 2]. [35],[36]Figure 2: RF/RHD associated HLA class II alleles:distribution around the world Several identifiedalleles by serology in the 80`s and/or molecularbiology after the 90`s were shown. Americas: (USA,Mexico, Martinique, South of Brazil); Asia:(Paquistan-Kashmir, North India, Latvia, Japan,South China), United Arab Emirates: (Saudi Arabia)Europe-Asia: (Turkey), Africa: (South Africa andEgypt)Click here to viewThe HLA-DR7 allele that was found in Brazilian, Turkish, Egyptian, and Latvian patients could be considered the HLA class II gene that is most consistently associated with RF/RHD. HLA-DR4 and -DR7 are associated with HLA-DR53 [Figure 2]. In addition, the association of HLA-DR7 with some HLA-DQB or -DQA alleles may be related to the development of multiple valvular lesions (MVL) in RHD patients in Egypt and in Latvia. [37],[38],[39]The molecular mechanism by which HLA class II molecules confer susceptibility to autoimmune diseases is not clear. As mentioned above, the role of HLA class II molecules is to present antigens to the TCR, leading to the recruitment of large numbers of CD4 + T cells that specifically recognize antigenic peptides from extracellular pathogens and the activation of adaptive immune responses. Therefore, the associated alleles probably encode molecules that facilitate the presentation of some streptococcal peptides to T cells that later trigger autoimmune reactions mediated by molecular mimicry.In summary, several alleles of the HLA class II genes appear to be the dominant contributors to the development of RF and RHD. Polymorphisms (SNPs and variable number of tandem repeat sequences of nucleotides) in genes involved with inflammatory responses and host defenses against pathogens that are associated with disease probably contribute to the development of valvular lesions and can determine the type of rheumatic valvular lesions(stenosis, regurgitation, or both) that occur in RHD patients.Rheumatic Fever and Rheumatic Heart Disease areMediated by Molecular Mimicry Between S.Pyogenes andHuman ProteinsMolecular mimicry between components of B hemolyticus streptococci and human heart tissues is the central problem in the pathogenesis of ARF and RHD. The precise mechanisms are being investigated for many years, and some real progress in the understanding of the pathogenesis is occurring slowly. [40],[41],[42],[43]Both T and B lymphocytes can recognize pathogenic and self antigens via four different types of molecular mimicry: (1) identical amino acid sequences, (2) homologous but non-identical sequences, (3) common or similar amino acid sequences of different molecules (proteins, carbohydrates) and (4) structural similarities between the microbe or environmental agent and its host.[43],[44] Autoimmune diseases from molecular mimicry may be facilitated because of the phenomena of epitope spreading and TCR degeneracy. Epitope spreading is the mechanism by which an ongoing immune response leads to reactivity against epitopes that are distinct from the original disease-inducing epitope [43],[45] and degeneracy of TCRs, which allows the recognition of a broad spectrum of antigens (self and microbial antigens) by the same T lymphocyte through it`s receptor. [41],[42],[46]The M protein is the most important antigenic structure of the S. pyogenes and shares structural homology with a-helical coiled-coil human proteins such as cardiac myosin, tropomyosin, keratin, laminin, vimentin and several valvular proteins. [40],[41],[42],[47]Several studies done in the last 50 years described the presence of cross-reactivity between human proteins and streptococcal antigens recognized by antibodies. [40] Among these human proteins, cardiac myosin and vimentin seem to be the major targets of cross-reactive reactions, along with other intracellular valvular proteins. N-acetyl ß-D-glucosamine, a polysaccharide present in streptococcal cell wall, induces cross-reactivity against laminin, an extracellular matrix alpha helical coiled-coil protein present in the valves. [40] By using affinity purified anti-myosin antibodies, Cunningham΄s group identified a five amino acid (Gln-Lys-Ser-Lys-Gln) epitope of the N-terminal M proteins of serotypes 5 and 6 (M5, M6) as being cross-reactive with cardiac myosin. [40]The interplay of humoral and cellular immune responses in RHD was recently demonstrated by Cunningham΄s group through two elegant studies. They showed that, in rheumatic carditis, antibodies that cross-react with streptococcal and human proteins bind to the endothelial surface and upregulate the adhesion molecule VCAM-1 [48] , leading to inflammation, cellular infiltration and valve scarring. [49] These data suggest that ARF may result from initial antibody mediated damage that later may be perpetuated by cell mediated inflammation. [50]Although antibodies in the sera of RF/RHD patients cross-react with several human proteins, we demonstrated that rheumatic heart disease lesions are mediated mainly by inflammatory cells and CD4 + T lymphocytes. [51]Studies performed in the last 25 years showed that CD4 + T cells are the major effectors of autoimmune reactions in the heart tissue in RHD patients. [51],[52],[53] The in vitro reactivity of peripheral T cells from RHD patients was evaluated in an early study that showed that these cells were able to recognize a 50- to 54-kDa myocardial protein fraction indicating autoreactivity to heart antigens, which was probably caused by streptococcal infection. [54] The role of T cells in the pathogenesis of RF and RHD was demonstrated through the analysis of heart-tissue infiltrating T cell clones. We demonstrated for the first time that M5 protein peptides (residues 81-96 and 83-103) displayed cross-reactivity with valvular proteins by molecular mimicry. [51] We also showed that valve-infiltrating T cells recognized cardiac myosin peptides by molecular mimicry and epitope spreading mechanisms. [55]These immunodominant M5 epitopes were preferentially recognized by peripheral T lymphocytes from RHD patients, when compared with normal individuals, mainly in the context of HLA-DR7. [56] These results suggested that autoreactive T cells migrate from the periphery to the site of heart lesions. Similarly, Yoshinaga et al. [57] reported that T cell lines derived from heart valve specimens and PBMC from RF and RHD patients react with cell wall and membrane streptococcal antigens. These lymphocytes, however, did not cross-react with the M protein or mammalian cytoskeletal proteins. [57]Recently, two studies demonstrated mimicry between cardiac myosin and the streptococcal M protein and pointed out different patterns of T cell antigen cross-recognition. One of them focused on peripheral T cell clones from one patient with RHD, which recognized different alpha helical coiled-coil proteins, such as the streptococcal M protein, myosin, laminin and tropomyosin. [58]The other study focused on the reactivity of intralesional T cell clones derived from myocardium and valvular tissue of six RHD patients against cardiac myosin, the streptococcal M5 protein and valve-derived proteins. A high frequency of reactive T cell clones was found (63%). These T cells displayed three patterns of cross-reactivity: (1) cardiac myosin and valve-derived proteins; (2) cardiac myosin and streptococcal M5 peptides; and (3) cardiac myosin, streptococcal M5 peptides and valve-derived proteins.[55]Using a proteomics approach, we showed that T cells recognize vimentin, further supporting the role of this protein as a putative autoantigen involved in rheumatic lesions. In addition, we identified myocardial and valvular autoantigens that were recognized by heart-infiltrating and peripheral T cells from RF/RHD patients. Novel heart tissue proteins were identified, including disulfide isomerase ER-60 precursor (PDIA3) protein and a 78-kDa glucose-regulated protein precursor (HSPA5). [59] However, their role in RHD pathogenesis and other autoimmune diseases is not clear.As mentioned above, both epitope spreading and the degeneracy of T cell receptors contributed to the amplification of cross-reactivity that leads to tissue damage.By using a molecular approach, we evaluated Vb chain usage by TCRs and the degree of clonality of heart-tissue infiltrating T cells. In RHD, the autoreactive T lymphocytes that infiltrate both the myocardium and the valves were identified in oligoclonal expansions by analyzing their TCRs. A high number of T cell oligoclonal expansions were found in the valvular tissue, indicating that specific and cross-reactive T cells migrate to the valves. [49]An effective immune response depends on cytokine production. CD4 + T helper cells are crucial regulators of the adaptive immune response. Antigen-activated CD4 + T cells become polarized toward a Th1 or Th2 phenotype based on the cytokines they secrete. Th1 cells are involved with cellular immune response and produce IL-2, IFN-γ and TNF-α. Th2 cells mediate humoral and allergic immune responses and produce IL-4, IL-5 and IL-13. A new lineage of CD4 + T cells (Th17) was recently described and is characterized by the production of IL-17. In vitro studies indicated a proinflammatory function for IL-17, and its expression was found to be associated with some inflammatory and autoimmune diseases. [60],[61]The role of cytokines in RF/RHD was first evaluated by examining the sera of patients and peripheral mononuclear cells stimulated by streptococcal antigens. These samples showed increased amounts of proinflammatory cytokines (IL-1, IL-6, TNF-a and IFN-g). [62] Immunohistochemistry on heart tissue (myocardium and valves) from acute and chronic RHD patients, showed a large number of mononuclear cells able to secrete TNF-a, IFN-g and the regulatory cytokine IL-10. Importantly, while a significant number of IL-4 + cells were found in the myocardium, these cells were very scarce in valve lesions in RHD patients. It is important to remember that valve damage and not myocarditis is the main problem in ARF. These observations indicated a role for balanced Th1/Th2 cytokines in healing myocarditis and in the induction of progressive and permanent valve damage. [29] IL-17 and Il-23 (Th17 cytokines) were recently analyzed by immunohistochemistry in both myocardium and valvular tissue from RHD patients. We observed a large number of IL-17 + and IL-23 + heart-tissue infiltrating cells (unpublished results), showing that these cytokines also play an important role in the development of heart lesions.Animal Models of RF/RHDHumans are unique hosts for S. pyogenes infections.Several studies (in mice, rats, hamsters, rabbits and primates) have been done to find a suitable animal model in which to examine the autoimmune process leading to RF/RHD with little success. [63] In the last decade, a model in Lewis rats has been developed that appears to be useful for the study of RF/RHD. These rats have already been used to induce experimental autoimmune myocarditis and study the pathogenesis of RF/RHD. [64],[65],[66]Immunization of Lewis rats with recombinant M6 protein induced focal myocarditis, myocyte necrosis and valvular heart lesions in three out of six animals. The disease in these animalsincluded verruca-like nodules and the presence of Anitschkow cells, which are large macrophages (also known as caterpillar cells), in mitral valves. Lymph node cells from these animals showed a proliferative response against cardiac myosin, but not skeletal myosin or actin. A CD4 + T cell line responsive to both the M protein and cardiac myosin was also obtained. Taken together, these results confirm the cross-reactivity between the M protein and cardiac myosin triggered by molecular mimicry, as observed in humans, possibly causing a break in tolerance leading to autoimmunity. [67],[68]Similarly, immunizing the Lewis rats with synthetic peptides from the conserved regions of M5 protein, or from B and C regions , or a recombinant M5 proteins have yielded focal myocarditis, infiltration with CD4+T cells, CD68 + macrophage but no typical aschoff`s nodule. [69],[70],[71],[72]Thus the Lewis Rat model could be considered a model of autoimmune valvulitis akin to ARF.Prospective Vaccines against S.PyogenesMany studies have focused on developing a vaccine against S. pyogenes in order to prevent infection and its complications. There are four anti-group A streptococci (GAS) vaccine candidates based on the M protein and eight more candidates based on other streptococci antigens, including group A CHO, C5a peptidase (SCPA), cysteine protease (Spe B), binding proteins similar to fibronectin, opacity factor, lipoproteins, Spes (super antigens) and streptococcal pili. [73]A multivalent vaccine, currently under phase II clinical trials, combines the amino acid sequences of the N-terminal portion of the M protein from the 26 most common strains of GAS in the US as a recombinant protein. [74],[75],[76]Because the C-terminal portion of the M protein is conserved among the 200 strains identified by their emm-types, vaccines based on this region are expected to provide broad coverage. The first attempt to develop a vaccine based on the C-terminal portion of the M protein was performed by Fischetti et al. [77] This vaccine was able to induce protection against S. pyogenes containing homologous (M6) and heterologous (M14) M protein, demonstrating that the use of conserved region-derived peptides could induce protection against different serotypes. [78]Conserved epitopes from the M protein have been also studied by a group from Australia, where the incidence of streptococcal infections in aboriginal communities is very high. Two synthetic peptides from the M5 protein (J8 and J14) were selected, and several formulations presented promising results. [79],[80],[81],[82] A combination of J8 and the fibronectin-binding repeats region (FNBR) of fibronectin I (SfbI) provided enhanced protection against S. pyogenes in mice. [83]We developed a vaccine epitope (StreptInCor) composed of 55 amino acid residues of the C-terminal portion of the M protein that encompasses both T and B cell protective epitopes. [84]The structural, chemical and biological properties of this peptide were evaluated and have shown that StreptInCor is a very stable molecule, an important property for a vaccine candidate. [85] Furthermore, experiments with mice showed that this construct is immunogenic and safe. [86]The greatest challenge for the development of a GAS vaccine resides in the promotion of immunity without generating cross-reactivity with human tissue. An effective and safe vaccine is still needed, most of all in developing countries.ConclusionSeveral genes involved in the control of infection and the immune response play a role in the development of RF and RHD. Some genes are associated with the innate immune response, and others with the adaptive immune response. Many of these genes are responsible for the inflammatory process and autoimmune reactions.In rheumatic carditis, antibodies that cross-react with streptococcal and human proteins upregulate adhesion molecules, leading to inflammation and increased cellular infiltration. CD4 + T cells that cross-react with heart tissue and streptococcal antigens are the major effectors of heart lesions.Large numbers of mononuclear cells that infiltrate rheumatic heart lesions produce inflammatory cytokines (TNF-a and IFN-g) and the imbalance between these cells and the IL-4-producing Th2 cells in the valve tissue might contribute to the progression and maintenance of rheumatic valvular lesions. Th17 cells also play a role in the development of autoimmunity.Several pathogenic M protein epitopes were identified that can induce cross-reactive responses against human proteins. Both epitope spreading and TCR degeneracy increase the possibility of cross-reactivity between infectious agents and self antigens.An animal model of Lewis rat displays similar heart lesions to RHD and is considered a good model of the disease.The development of a vaccine against S. pyogenes is an important goal and, given the number of ongoing studies, will probably be a reality in the near future.。

护理医学英语教学法分析与研究性论文在多年的对英语写作的教学方法的不断的探索和研究中，一系列的理论和教学实践发展比较成熟、具有一定影响的教学方法应运而生，主要包括:成果教学法、过程教学法和体裁教学法等。

2000年RichardBadger和GoodithWhite提出了过程体裁教学法，旨在将成果教学法、过程教学法和体裁教学法三者的优势相结合，为英语写作教学提供了新的视角和思路。

不少研究者(秦秀白2000;韩金龙xx;周雪xx等)［1～3］等都对此进行了理论探讨，后来的研究者(沈玉如xx;丁铭xx;何晓嘉xx等)［4～6］还就过程体裁教学法运用于大学专业英语或公共英语的写作教学进行了不少的实证研究，但相对而言，实证研究的案例少，实验周期短(一般一个学期)，样本小(最多60人左右)，代表性不强，操作步骤比较随意，得出的结果不能完全体现所要达到的验证目的。

同时医学英语写作由于专业性强，教材不足或不够成熟的原因，过程体裁教学法的运用则鲜有探讨和实证研究。

本文将探讨过程体裁教学法写作教学模式应用于护理医学英语写作教学的可行性，并结合笔者的教学实践，总结出具体的、可操作的适应于护理医学学生特点的写作教学模式。

在大学英语教学实践中不断完善过程体裁教学法的观念，探索更多的写作应用模式，并且加大实证研究成为必然。

1．护理医学英语写作教学中的不足护理医学英语写作专业性很强，同时受传统的成果教学法的影响，日常临床护理英语语篇写作教学在护理医学英语写作中一直被有意或无意地回避和忽视。

结果表现为学生不能熟练理解和创作符合日常护理工作的特定体裁的英语语篇文书，对护理工作的日常交往需求准备不足。

从课堂表现来看，学生缺乏良好的写作习惯，语言表达能力差，内容空洞，缺乏创造性的思维模式，写作兴趣索然。

2．过程教学法和体裁教学法在护理医学英语写作教学中的不足(1)过程教学法过程教学法始于20世纪60年代，深受认知理论和交际教学法的影响，是由Graves(1978)提出的。

对我院医学专业大学生专门用途英语教学的探究选择医学专业的本科学生在完成大学英语学习基础阶段后，面临着更高级的外语学习及专业外语学习。

通过对加强专门用途英语教学的必要性和可行性的再认识，明确基础英语教学和专门用途英语教学的实质，提出加强我院专门用途英语教学的建议和措施。

大学英语专门用途英语医学英语一、我国大学英语教学现状我国的高等医学院校的学生在大学英语基础阶段的学习和其他专业一样，使用全国统一的教学大纲，统一教材，统一进度，统一评估标准。

即大学一、二年级的主要目标是打下坚实的语言基础，培养语言交际的基本能力。

争取在全国统一的大学英语四、六级考试中取得好成绩是绝大多数学生孜孜以求的目标，在这一点上，医学生也不例外。

但是，修订后的《大学英语教学大纲》于1999年问世，新大纲对大学英语的教学提出了比以往更高的要求，而且新大纲正式提出了“专业英语”的名称。

“专业英语”的概念产生于第二次世界大战后的上个世纪60年代初期，当时许多国家正面临着严峻的挑战。

他们需要摆脱战争所带来的困境，重振经济、发展科技、加强国际间的交流。

而英语在当时已被认为是科技和商贸领域里的国际语言。

人们学习英语的主要目的是把英语作为一种工具，为自己所从事的专业服务，创造美好的职业生涯。

在这种背景下，语言学家们开始注重专门英语(english for special purpose)的教学。

对于大学基础英语教学，新《大纲》规定：“基础阶段词汇量基本要求和较高要求分别为4200和5500”。

应该说，完成了基础英语学习的学生的语言知识和技能已经达到了相当的程度，完全可以开展esp教学。

另外，不同专业的学生对英语学习的要求侧重于不同方面，从学生专业发展的角度来看，他们也需要提高与自己本专业密切相关的专业英语水平，这就产生了对专业英语学习的需求。

但是，究竟该如何规划、实施esp教学，需要教育管理者和教学实践者自己来进行。

因为医学专业知识的博大精深，自成体系，使得医学专业的大学生很有必要在具备一般英语知识的基础上，学习浩如烟海的医学英语知识，所以要跟上形势的发展，适应学生的需要，满足社会的需求，必须对教学计划和教学材料进行经常性的检查和评估，随时调整我们的教学内容和手段，真正做到以学生为中心。

[医学英语文章带翻译]医学类英语文章医学英语文章带翻译医学英语文章带翻译医学英语文章带翻译 1 椎间盘突出Unit 2 Text A Herniated Disc (Disc Herniation of the Spine) 第二单元主题 A 椎间盘突出症Many patients with back pain, leg pain, or weakness of the lower extremity muscles arediagnosed with a herniated disc. 许多患腰腿疼痛，下肢肌端乏力的病患均为椎间盘突出症。

When a disc herniation occurs, the cushion that sits between the spinal vertebra is pushedoutside its normal position. 椎间盘突出发生时，脊柱间的缓冲带将发生侧突。

A hrniated disc would not be a problem if it weren“t for the spinal nerves that are very close tothe edge of these spinal discs. 如果脊神经不是离椎间盘特别近的话，椎间盘突出就不是什么大问题了。

HOW ARE THE SPINE AND ITS DISCS *****D 脊柱与椎间盘The vertebras are the bony building blocks of the spine. 脊椎是建造脊柱的构件。

Between each of the largest parts (bodies) of the vertebrae are the discs. 各椎骨之间为椎间盘。

Ligaments are situated around the spine and discs. 脊椎和椎间盘周围散布着韧带。

基础医学专业英语文章范文The field of basic medical science encompasses a wide range of disciplines that form the foundation of modern healthcare. From anatomy and physiology to biochemistry and microbiology, these fundamental areas of study provide the essential knowledge and understanding required to effectively prevent, diagnose, and treat various medical conditions. In this essay, we will explore the importance of basic medical science and its role in advancing the medical profession.Anatomy and Physiology: The Building Blocks of the Human Body Anatomy and physiology are the cornerstones of basic medical science, as they delve into the structure and function of the human body. Anatomy focuses on the identification and description of the various organs, tissues, and systems that make up the body, while physiology examines how these components work together to maintain homeostasis and facilitate the body's vital processes.Understanding the intricate details of human anatomy is crucial for medical professionals, as it allows them to accurately diagnose andtreat a wide range of medical conditions. From identifying the location of a fracture to understanding the complex neurological pathways, a comprehensive knowledge of anatomy is essential for effective patient care. Furthermore, the study of physiology provides insights into the body's regulatory mechanisms, enabling healthcare providers to develop targeted interventions and therapies.Biochemistry: The Chemical Basis of LifeBiochemistry is another fundamental discipline within basic medical science, as it explores the chemical processes that underlie the functioning of living organisms. This field of study examines the structure and behavior of biomolecules, such as proteins, lipids, carbohydrates, and nucleic acids, and how they interact to sustain life.Understanding the biochemical mechanisms that govern the body's cellular processes is crucial for developing new diagnostic tools and therapeutic strategies. For example, the study of enzyme kinetics and drug-target interactions can lead to the development of more effective medications, while the analysis of genetic and metabolic pathways can help identify biomarkers for early disease detection.Microbiology: The Invisible Realm of Infectious Agents Microbiology, the study of microscopic organisms, is a crucial component of basic medical science. This field encompasses the investigation of bacteria, viruses, fungi, and other microbes, and theirrole in human health and disease.The knowledge gained from microbiology research is essential for the prevention, diagnosis, and treatment of infectious diseases. By understanding the characteristics, transmission, and pathogenesis of various microorganisms, healthcare professionals can develop effective infection control measures, design targeted antimicrobial therapies, and implement appropriate public health strategies.Furthermore, the study of the human microbiome, the complex community of microbes that reside within the human body, has emerged as a rapidly growing area of research in basic medical science. Insights into the role of the microbiome in maintaining health and its potential involvement in the development of various diseases have opened up new avenues for therapeutic interventions and personalized medicine.Immunology: The Body's Defense SystemImmunology, the study of the immune system, is another crucial component of basic medical science. This field examines the complex mechanisms by which the body recognizes and responds to foreign substances, such as pathogens and allergens, to maintain homeostasis and prevent disease.Understanding the intricate workings of the immune system isessential for the development of effective vaccines, immunotherapies, and treatments for autoimmune disorders. By elucidating the cellular and molecular pathways involved in immune responses, researchers in basic medical science can contribute to the advancement of medical interventions that harness the body's natural defenses to combat a wide range of health challenges.Pathology: Unraveling the Mysteries of DiseasePathology, the study of the underlying causes and effects of diseases, is a fundamental discipline within basic medical science. This field encompasses the investigation of the structural and functional changes that occur in cells, tissues, and organs during the course of a disease, as well as the identification of the factors that contribute to the development and progression of various medical conditions.The knowledge gained from pathological research is crucial for accurate diagnosis, effective treatment, and the development of preventive strategies. By understanding the pathogenesis of diseases, healthcare professionals can design more targeted and personalized interventions, leading to improved patient outcomes.Translational Research: Bridging the Gap between Basic Science and Clinical PracticeThe ultimate goal of basic medical science is to translate the knowledge and insights gained from fundamental research intopractical applications that can benefit patient care. This process, known as translational research, involves the collaborative efforts of basic scientists, clinicians, and other healthcare professionals to ensure that the advancements in basic science are effectively integrated into clinical practice.Through translational research, new discoveries in areas such as genetics, molecular biology, and pharmacology can be transformed into novel diagnostic tools, therapeutic interventions, and preventive strategies. This bidirectional flow of information between the laboratory and the clinic is essential for advancing the medical field and improving the overall health and well-being of patients.ConclusionIn conclusion, basic medical science is the foundation upon which the medical profession rests. By exploring the fundamental aspects of human biology, biochemistry, and microbiology, researchers and healthcare professionals can gain a deeper understanding of the mechanisms underlying health and disease. This knowledge is essential for the development of effective diagnostic tools, therapeutic interventions, and preventive strategies, ultimately leading to improved patient outcomes and the advancement of the medical field as a whole.。

Abstract: objective to study of TNF alpha Ghrelin human brain microvascular endothelial cells induced (HBMEC) mononuclear cells chemotaxis protein 1 (MCP-1) influence and p38MAPK role. Methods HBMEC training, TNF alpha group to join different concentration TNF alpha; Ghrelin pretreatment section first join Ghrelin pretreatment 1 h, then add the TNF alpha. The RT-PCR method to detect MCP-1 mRNA level, immune imprinting method to detect p38 phosphorylation (p-p38) expression. The results of the TNF alpha stimulation, MCP-1 mRNA express obvious enhancement, and the concentration of a certain dose-response relationship (P < 0.05) in the cytoplasm and P-p38 protein expression also significantly increased (P < 0. 05). Ghrelin pretreatment can reduce MCP-1 mRNA cytoplasm and the p-p38 protein expression (p < 0. 05). Conclusion Ghrelin may inhibit p-p38 pathways inhibit TNF alpha mediated HBMEC MCP-1 mRNA expressions.Keywords: mononuclear cells chemotaxis protein 1; The human brain microvascular endothelial cells; GhrelinIn recent years, and the relationship between Ghrelin inflammation is paid attention to, but for inflammation, Ghrelin in different tissues function is not the same, need to make clear further [1 ~ 5]. April 2008 to July 2009, we studied Ghrelin TNF alpha induction of the human brain microvascular endothelial cells (HBMEC) mononuclear cells chemotaxis protein 1 (MCP-1) phosphorylation mRNA and p38 (p-p38) the influence of the expression, this paper discusses Ghre-Lin in the possible anti-inflammatory mechanism vessel, as Ghrelin applied to clinical diabetes cerebrovascular disease and provided the reference.1 materials and methods1.The human brain microvascular endothelial cell lines 1 materials HBMEC Scien cell bought in the United States, rhTNF alpha Sigma company bought in, TaKaRaRNA PCR Kit (AMV) V er. 3. 0 bought in dalian treasure biological engineering Co., LTD, p-p38MAPK mice monoclonal antibodies against human bought in Santa Cruz company, other drugs for the sold analysis pure.1. 2 method1. 2. 1 cells culture and group HBMEC cells use tire bovine serum containing 5% of 37 ℃ and 5% in DMEM CO2Humidity under cultivation, and pancreatic enzyme digestion ChuanDai, the fusion status for the experiment. With 5 x 105 / hole vaccination to 6 orifice plate, to 90% fusion, serum-free culture 24 h, PBS cleaning 2 times, join condition culture medium: TNF alpha (0. 1, 1, 10 ng/ml) or Ghrelin (1, 10, 100 ng/ml) effect 24 h.Ghrelin pretreatment section first join Ghrelin (10 ng/ml) pretreatment 1 h, then add the TNFalpha, and the concentration of 1. 0 ng/ml, training 24 h, abandon medium to join TRIzol reagent, cracking cells, extraction RNA.1. 2. 2 MCP-1 mRNA express detection using total RNA extraction reagent TRIzol, cells extracted total RNA, uv spectrophotometer measurement sample spectrophotometry, A260 / A280 nm should be in 1: ~ 2. 0. Primer according to GenBank middleman MCP-1 cDNA sequence design, MCP-1 upstream: 5 'GCTCGCTCAGCCAGATGCAAT-3 ', downstream: 5 'TGGGTTGTGGAGTGAGTGTTC-3 ', the expansion of section for 257 bp; Beta actin on tour: 5 'AAATCGTGCGTGACA T-TAA-3 ', downstream: 5 'CTCGTCATACTCCTGCTTG-5', amplification clips for 473 bp. RT-PCR concrete operation according to illustrate kit. Drug synthesis cDNA reaction conditions: 30 ℃10 min, 42 ℃30 min, 99 ℃10 min, 5 ℃5 min. Synthesis of making cD with primer for corresponding amplification. Expansion conditions for 94 ℃the degeneration 2 min, with 94 ℃degeneration 1 min, 57 ℃annealing 1 min. 72 ℃extensions 1 min, a total of 30 circulation, 72 ℃extensions 10 min. PCR products by 1. 5% agarose gel electrophoresis gel after imaging system analysis. Light density scanner light density detection, and with MCP-1 mRNA and beta actin mRNA said the ratio of the relative value of making the mR. Take control of the relative expression for 1, each of the relative amount compared with the expression with multiple of said.1. 2. 3 p-p38 protein expression detection with 100 ng/ml Ghrelin pretreatment cell 1 h joined after 10 ng/ml of TNF alpha, cultivate 30 min respectively, collect cells, extraction protein, immune imprinting method to detect p-p38, beta actin expression. With p-p38 and beta actin density of the ratio of the said purpose the relative content of protein, the relative expression for the control group of 1, each of the relative amount compared with the expression with multiple of said.1. 2. 4 statistical methods using SPSS 13. 0 software comparison between groups, measurement data with 珋x ± s said, compares the two two LSD method. With P than 0. 05 for statistically significant.2 the results2. 1 MCP-1 mRNA without the express HBMEC cells stimulate MCP-1 mRNA expression level is low, TNF alpha stimulation, MCP-1 express obvious enhancement, the concentration of a certain dose-response relationship (P < 0. 05), see figure 1. Ghrelin alone to MCP-1 role to express the impact is not big, but Ghrelin pretreatment can reduce TNF alpha induction of MCP-1 mRNA expression (P < 0. 05), see figure 2.2. 2 p-p38 Ghrelin protein expression of TNF alpha induction of cytoplasmic p-p38 protein expression influence the results shown in figure3. The figure 3 shows, normally, HBMEC cytoplasmic express certain p-p38 protein that TNF alpha stimulate 30 min, the cytoplasmic p-p38 protein significantly increased, and Ghrelin separate function group p-p38 protein expression the normal group is less; Ghrelin pretreatment group in the cytoplasm p-p38 protein is TNF alpha group reduce (p < 0. 05).3 discussThere is evidence that the metabolic syndrome in express MCP-1, TNF alpha channel have special role. To determine whether the endothelial Ghrelin cerebrovascular modulate inflammatory factor MCP-1 secretion, we tested the Ghrelin of MCP-1 mRNA influence. The results showed that TNF alpha obviously increase the human brain microvascular endothelial cell lines HBMECMCP-1 mRNA expression, its may be obese patients with insulin resistance to get one of the causes of the cerebral arteriosclerosis. Ghrelin can restrain the foundation and TNF alpha induction of MCP-1 mRNA expression, prove its can inhibit endothelial inflammatory factor expression of cerebral function, this is Ghre-Lin independent of adjusting glucolipid metabolism outside of the role, is also the main points of the study. PetCO2 monitoring. For patients with lung disease, lung disease will delay the potential CO2 to eliminate, more should be extended breath support after the time. This kind of patients PetCO2 mild increase and was not accurate in reflecting artery blood high CO2 and respiratory acidosis degree, the determination of the Pet-CO2 value and the blood PaCO2 correlation is not good. Postoperative premature dial to the spontaneous breathing easy appear hypercapnia and acidosis, should first selection arterial blood gas monitoring. The CO2 gasless laparoscopic led to internal pressure within the chest and pressure, blood vessels active substances such as catecholamine and vasopressin release increase, hypercapnia evoked the sympathetic nervous tension increased. Can cause significant hemodynamic changes. We in the study also found that patients and stop after gasless laparoscopic 15, pp 30 min SBP before a clinical increases, and HR and DBP over time points, DBP SBP and HR is a slightly elevated before pp, but no clinical significance. May the choice of case and case and intraoperative strict management relevant, patients with no serious disease, maintain enough depth of anesthesia, ensure analgesia and perfect control gasless laparoscopic relatively low pressure are perioperative blood flow dynamics of the important factors less jerky. This also with our previous observation results are basically the same. Elderly patients for clinical operation cycle reflect mainly displayed in the SBP on the rise of the concrete reason is not very clear, pending further study.In conclusion, we through to over 60 patients after laparoscopic study found that, between PetCO2 and PaCO2 are good for the correlation. PetCO2 can be accurate guide intraoperative breathing management, after laparoscopic gasless laparoscopic in elderly patients. The influence of the SBP obviously, perioperative should pay attention to monitoring and handle in time.Reference：1：Soubani AO．Noninvasive monitoring of oxygen and carbon dioxide［J］．Am J Emerg Med，2001，19( 2) : 141-146．2：杨明华，林智平，叶允荣．不同潮气量机械通气下肺癌根治术病人动脉血二氧化碳分压与呼气末二氧化碳分压的关系［J］．中华麻醉学杂志，2006，26( 1) : 86-87．3：Klopfenstein CE，Schiffer E，Pastor CM，et al．Laparoscopic colonsurgery: unreliability ofend-tidal CO2monitoring ［J］．Acta Anaes-thesiol Scand，2008，52( 5) : 700-707．4：Yosefy C，Hay E，Nasri Y，et al．End tidal carbon dioxide as a pre-dictor of the arterial PCO2in the emergency department setting ［J］．Emerg Med J，2004，21( 5) : 557-559．5：Bhavani-Shankar K，Steinbrook RA，Brooks DC，et al．Arterial toend-tidal carbon dioxide pressure difference during laparoscopic sur-gery in pregnancy ［J］．Anesthesiology，2000，93( 2) : 370-373．6：Meininger D，Westphal K，Bremerich DH，et al．Effects of postureand prolonged pneumoperitoneum on hemodynamic parameters dur-ing laparoscopy ［J］．World J Surg，2008，32( 7) : 1400-1405．7：Streich B，Decailliot F，Perney C，et al．Increased carbon dioxideabsorption during retroperitoneal laparoscopy ［J］．Br J Anaesth，2003，91( 6) : 793-796．［8］韩文勇，李水清，李民，等．高龄患者后腹腔镜手术的麻醉管理［J］．中国微创外科杂志，2007，7( 10) : 971-973．以上文章由代写教育论文网 发表转载请注明。

医学英语关于疾病的作文Title: Understanding Common Diseases: A Brief Overview in Medical English。

In today's rapidly advancing world, understanding common diseases is imperative for both medical professionals and the general public. Diseases can affect individuals of all ages, genders, and backgrounds, often causing significant health challenges. In this essay, we will explore several prevalent diseases, their symptoms, causes, and potential treatments, all presented in medical English.1. Diabetes Mellitus。

Diabetes mellitus, commonly referred to as diabetes, is a chronic metabolic disorder characterized by elevated blood sugar levels over a prolonged period. There are two primary types: type 1 and type 2 diabetes.Symptoms: Increased thirst, frequent urination, unexplained weight loss, fatigue, blurred vision, and slow wound healing.Causes: Type 1 diabetes results from the immune system mistakenly attacking insulin-producing beta cells in the pancreas, while type 2 diabetes develops due to insulin resistance and insufficient insulin production.Treatment: Management involves lifestyle modifications such as dietary changes, regular exercise, oral medications, insulin therapy, or a combination thereof.2. Hypertension (High Blood Pressure)。

医疗研究作文英语Medical Research。

Medical research plays a crucial role in improving healthcare and finding cures for various diseases. It involves the investigation of new treatments, drugs, and medical technologies to enhance the quality of life for individuals and communities. In this essay, we will explore the significance of medical research and its impact on society.Firstly, medical research contributes to the development of new treatments and drugs that can save lives and alleviate suffering. Through rigorous scientific studies and clinical trials, researchers can identify effective therapies for diseases such as cancer, diabetes, and cardiovascular disorders. For example, the discovery of antibiotics revolutionized the treatment of bacterial infections and saved countless lives. Medical research also leads to the development of vaccines that preventinfectious diseases, such as polio, measles, and influenza. These advancements have had a profound impact on public health and have contributed to the eradication of deadly diseases.Furthermore, medical research plays a critical role in understanding the underlying causes of diseases and identifying risk factors that can inform preventive measures. By studying the genetic, environmental, and lifestyle factors that contribute to disease development, researchers can develop strategies to reduce the burden of illness in populations. For instance, studies on the link between smoking and lung cancer have led to public health campaigns that promote smoking cessation and tobaccocontrol policies. Medical research has also shed light on the importance of healthy eating and physical activity in preventing chronic diseases such as obesity, diabetes, and heart disease.In addition, medical research drives innovation in healthcare by fostering the development of new medical technologies and diagnostic tools. Advanced imagingtechniques, such as MRI and CT scans, enable healthcare providers to visualize internal organs and detect abnormalities with greater precision. Moreover, the use of artificial intelligence and big data analytics has the potential to revolutionize the diagnosis and treatment of diseases by identifying patterns and trends in large datasets. These technological advancements have thepotential to improve patient outcomes and streamline healthcare delivery.Medical research also has a significant economic impact, as it contributes to the growth of the pharmaceutical and biotechnology industries. The development of new drugs and medical devices not only creates jobs and stimulates economic growth but also generates revenue for healthcare providers and pharmaceutical companies. Moreover, medical research attracts investment in healthcare infrastructure and fosters collaboration between academia, industry, and government agencies. This collaboration is essential for translating research findings into clinical practice and ensuring that patients benefit from the latest advancements in medical science.In conclusion, medical research is a cornerstone of modern healthcare and has far-reaching implications for individuals, communities, and societies. By advancing our understanding of disease mechanisms, developing new treatments, and driving innovation in healthcare, medical research has the potential to improve the quality of life for millions of people around the world. Therefore, it is essential to support and invest in medical research to address the healthcare challenges of the 21st century.。