I do solemnly swear by that which I hold most sacred that I will be loyal to the profession of medicine and just and generous to its members; that I will lead my life and practice my art in uprightness and honor; that into whatsoever house I shall enter, it shall be for the good of the sick and the well, to the utmost of my power; that I will hold myself aloof from wrong, from corruption, from tempting of others to vice; that I will exercise my art solely for the cure of my patients and the prevention of disease; that I will give no drug, perform no operation for a criminal purpose, far less suggest it; that whatsoever I shall see or hear of the lives of men, which is not fitting to be spoken, I will keep inviolably secret. These things I do promise, and in proportion as I am faithful to this my oath, may happiness and good repute be ever mine; the opposite if I shall be foresworn.

Drug Therapy： Hepatitis B Virus Infection

乙肝病毒感染的药物治疗 （原文发表于2008年10月的NEJM）

Jules L. Dienstag, M.D.

Reports of successful antiviral therapy for chronic hepatitis B virus (HBV) infection appeared three decades ago,¹ and during the past decade, progress has accelerated dramatically. Along with progress, however, has come complexity. So much more is known now than at the dawn of the antiviral era about the protean clinical expressions of HBV infection that determining whom, when, and how to treat has become progressively more challenging.

成功的乙肝抗病毒治疗已经出现了几十年，但是随着对HBV认识的增加，其感染后的临床表现使哪些感染者，什么时候以及怎样接受治疗变得越发困难

Virologic and Epidemiologic Factors and Natural History  

病毒及流行病学因素以及疾病自然史

HBV, a DNA virus transmitted percutaneously, sexually, and perinatally, affects 1.25 million persons in the United States and 350 to 400 million persons worldwide. HBV infection accounts annually for 4000 to 5500 deaths in the United States and 1 million deaths worldwide from cirrhosis, liver failure, and hepatocellular carcinoma.^2,3,4,5,6  

乙肝病毒经皮肤？，性生活，和围产期哺乳传播，全世界有3.5到4亿感染者，导致世界范围内每年有100万患者死于肝硬化，肝衰和肝细胞癌

Viral proteins of clinical importance include the envelope protein, hepatitis B surface antigen (HBsAg); a structural nucleocapsid core protein, hepatitis B core antigen (HBcAg); and a soluble nucleocapsid protein, hepatitis B e antigen (HBeAg). Serum HBsAg is a marker of HBV infection, and antibodies against HBsAg signify recovery. A serum marker  of active viral replication, HBeAg, is accompanied by serum levels of HBV DNA that are 100,000 to 1 million IU per milliliter or higher. HBV relies on a retroviral replication strategy (reverse transcrīption from RNA to DNA),⁷ and eradication of HBV infection is rendered difficult because stable, long-enduring, covalently closed circular DNA (cccDNA) becomes established in hepatocyte nuclei and HBV DNA becomes integrated into the host genome (Figure 1).  

具有临床意义的病毒蛋白包括包膜蛋白，乙肝表面抗原，结构性核衣壳核心蛋白，乙肝核心抗原，以及一可溶性核衣壳蛋白，乙肝e抗原。HBsAg表明乙肝病毒感染，HBeAg的出现意味着乙肝病毒DNA复制达到10万到100万，乙肝病毒的复制是逆转入，其中会产生稳定的共价闭合环状DNA整合到患者自身的的基因组。

Progression from acute to chronic HBV infection is influenced by the patient's age at acquisition of the virus; age is also related to a dichotomy in the clinical expression of HBV infection between high-prevalence (e.g., Asian) and low-prevalence (e.g., Western) countries (Figure 2). In the Far East, where HBV infection is acquired perinatally, the immune system does not recognize a difference between the virus and the host, and high-level immunologic tolerance ensues. The cellular immune responses to hepatocyte-membrane HBV proteins that are associated with acute hepatitis do not occur, and chronic, usually lifelong infection is established in more than 90% of persons who are infected. In contrast, in the West, most acute HBV infections occur during adolescence and early adulthood because of behavīors and environments that favor the transmission of bloodborne infections, such as sexual activity, injection-drug use, and occupational exposure. In immunocompetent adults, a strong cellular immune response to "foreign" HBV proteins expressed by hepatocytes results in clinically apparent acute hepatitis, which, in all but approximately 1% of persons infected, affects clearance of the infection.^5,6,8

急慢性肝炎的转变受患者感染病毒的年龄影响。在远东（中国），乙肝病毒的感染多发生在婴儿围产期，90%以上的婴儿的感染都会是慢性的终身的。但是在西方，乙肝病毒感染多发生在青少年时期导致急性肝炎，但是只有1%左右的人会感染。

Immunologic tolerance to HBV established during perinatal infection is profound and lifelong, but not complete; a low level of liver injury occurs and accounts for up to a 40% lifetime risk of death from liver disease among men.⁹ This risk is lower among women.⁹ A so-called immune-tolerant phase occurs in the early decades of life, with negligible HBV-associated liver injury despite high-level HBV replication. An immune-clearance phase occurs in the later decades of life with active liver disease. This categorization of phases reflects relatively higher immunologic tolerance early and relatively lower tolerance later in the natural history of chronic HBV infection acquired early in life.^5,6,10 Such categorization, however, does not explain the presence of substantial liver injury and fibrosis during the apparent immune-tolerant period in some patients^11,12 or the presence of necroinflammatory quiescence during the immune-clearance phase later in the course of chronic HBV infection.

围产期婴儿的感染所产生的免疫耐受是很明显的，也是终身的，但是并不彻底。它仍然会导致肝脏的轻度损伤，高达40%的男性感染者最终会因为乙肝病毒感染所导致的肝脏疾病而死亡，但是这个比率在女性低。这些感染者的早年会经历免疫耐受期，此段时间，感染者体内的病毒复制很高但是HBV相关的干损伤几乎没有。但是最后，这些感染者会经历一个免疫清除期，此段时间里，患者会活动的肝脏疾病。此疾病自然史，并没能解释在免疫耐受期，感染者仍存在实质性干损伤和肝纤维化，也没能解释在免疫清除期，为什么会有炎症坏死的静止期。

The HBeAg status distinguishes two additional categories of chronic HBV infection. HBeAg-reactive chronic HBV infection is accompanied by high-level HBV replication, and spontaneous seroconversion from HBeAg-positive to antibody (anti-HBe)–positive infection coincides with a reduction in HBV replication and clinical improvement.^13,14,15 HBeAg-negative chronic HBV infection, in which precore or core-promoter gene mutations preclude or reduce the synthesis of HBeAg, accounts for an increasing proportion of cases.¹⁶ Patients with HBeAg-negative chronic HBV infection tend to have progressive liver injury, fluctuating alanine aminotransferase (ALT) activity, and lower levels of HBV DNA than patients with HBeAg-reactive HBV infection; however, they cannot have treatment-induced HBeAg seroconversion, a durable response that may permit the discontinuation of antiviral therapy.

根据乙肝表面抗原，乙肝又分HBeAg阳性和HBeAg阴性。HBeAg阳性德慢性乙肝患者可以受益于HBeAg血清转化疗法和HBeAg抗体，但是HBeAg阴性患者不能益于HBeAg血清转化疗法，他们有进展的肝损害，变化的血清谷丙转氨酶，低溶度的HBV DNA（相对于HBeAg阳性患者）。

Eight HBV genotypes — and differences in clinical outcome according to genotype — are recognized.^17,18,19 For example, patients with genotype A are  more likely to undergo interferon-induced HBeAg seroconversion²⁰; HBeAg seroconversion and slower disease progression are more frequent in patients with genotype B than in patients with genotype C.¹⁹ These differences, however, are not sufficiently established to guide management.

HBV共有8种基因型，临床治疗效果取决于患者HBV的基因型。例如，A型患者更多地会接受干扰素诱导的HBeAg血清转化疗法，B型中的HBeAg血清转化疗法和病情缓解较C型好。但是仍不足以指导临床应用。

The progression of liver disease in HBV infection is fostered by active virus replication, reflected by the presence in serum of an HBV DNA level above a threshold of approximately 1000 to 10,000 IU per milliliter. Persons with a serum HBV DNA level below 1000 IU per milliliter and a normal ALT level consistently are considered to be inactive carriers with a low risk of clinical progression,²¹ although, rarely, reactivation can occur spontaneously or with immunosuppression.^22,23 Although perinatal infection can result in high-level HBV replication without substantial liver injury in the early decades of life, ultimately the risk of progression to cirrhosis and hepatocellular carcinoma is proportional to the level of HBV DNA maintained persistently over time.^24,25

肝脏的损害和其DNA复制成正比，血清HBV DNA溶度高于1000 到1万单位反映肝损害进展。而低于1000单位表示为隐性携带者.尽管围产期感染者最初表现为免疫耐受，其DNA容度高但是肝脏多无实质性损害，但是最终的肝硬化和肝细胞癌的进展情况仍与DNA量呈比例

Goals of Antiviral Therapy

抗病毒治疗目标

Because clinical and histologic improvement accompanies reductions in HBV replication, interventions that reduce HBV replication are expected to limit progressive liver disease and improve the natural history of chronic HBV infection. Practically, however, serious outcomes of HBV infection evolve over decades, whereas clinical trials of antiviral therapy are limited to 1 to 2 years and, rarely, up to 5 years. Therefore, surrogate end points that are achievable during time-limited clinical trials are used. These end points are serologic (i.e., HBeAg loss or seroconversion, usually reflecting a transition to inactive HBV carriage, and, more rarely, HBsAg loss or seroconversion, representing serologic recovery), virologic (i.e., a log₁₀ reduction in the HBV DNA level or suppression of HBV DNA to an undetectable level [<10 to 100 IU per milliliter]), biochemical (i.e., normalization of the serum ALT level), and histologic (i.e., improvement in the necroinflammatory grade and stage of fibrosis).^5,6 A course of antiviral therapy may lead to responses that are sustained after treatment withdrawal; more commonly, therapy must be continued to maintain responses achieved during therapy.  

因为肝炎病毒复制数的降低伴随着肝炎患者临床症状和组织学结构的改善，所以减少肝炎病毒复制是治疗的目标。但是事实上，因为肝炎的严重结局通常需要数十年，而临床药理实验通常为1到两年，很少有到5年的。所以替代性的结局指标被采用。这些替代指标包括血清学（如HBeAg的消失或血清转化通常表明患者转变成静息的肝炎病毒携带者，当然也有极少部分代表患者血清意义上的康复）、病毒学、生化和组织学指标。一个疗程的抗病毒治疗可以在停止治疗后仍然发挥作用，但是更常见的是治疗应该持续以维持疗效。

Antiviral Drugs

抗病毒药物

Seven drugs are licensed in the United States for the treatment of HBV infection: interferon alfa,^26,27,28,29 pegylated interferon alfa-2a,^30,31 lamivudine,^{32,33,34,35,36} adefovir,^{37,38,39,40,41} entecavir,^{42,43,44,45,46} telbivudine,^47,48,49 and tenofovir^50,51 (Table 1 and Table 2).^5,6,52 The use of interferon, which requires injections daily or thrice weekly, has been supplanted by long-acting pegylated interferon, which is injected once weekly.

在美国有七种药物允许上市用于治疗乙肝病毒感染，他们是：a干扰素，pegylated interferon alfa-2a，拉米夫定，adefovir, entecavir, telbivudine, tenofovir⁵⁰。干扰素因其需要每天或者每周三次注射已经被长效pegylated 干扰素（每周只需注射一次）所取代。

As shown in Table 1 and Table 2, treatment for 1 year generally results in the reduction of serum HBV DNA levels by 3.5 to 6.9 log₁₀, a level of serum HBV DNA that is undetectable by polymerase chain reaction in 13 to 95% of patients, normalization of the ALT level in 38 to 79% of patients, histologic improvement in 38 to 74% of patients, and HBeAg seroconversion in 12 to 27% of patients; drugs that suppress HBV DNA more profoundly more often achieve clinical end points (except perhaps HBeAg seroconversion). Among the oral agents, which differ in resistance profile, the nucleotide analogues adefovir and tenofovir are not cross-resistant with lamivudine, telbivudine, or entecavir. Adefovir resistance is negligible during the first year of therapy but approaches 30% by the end of 4 years. Adefovir is very effective in lamivudine-resistant HBV infection.^{37,38,39,40,53,54,55} Limiting its appeal among the available drugs, adefovir is the least potent, the slowest to suppress HBV DNA levels, the least likely to induce HBeAg seroconversion, and the most likely to result in "primary nonresponse" (i.e., failure to achieve a reduction in the HBV DNA level of 2 log₁₀ in 20 to 50% of patients⁵⁶).

在抗病毒治疗一年以后，血清PCR病毒检测有13%到95%的病人乙肝病毒DNA是阴性的，38-79%的病人谷丙转移酶是正常的，38-74%的病人的组织结构得到改善，12-27%的患者HBeAg发生血清转换。强效抑制HBV DNA的药物更易达到临床疗效指标要求（HBeAg血清转换除外）。口服抗病毒药物主要是存在药物抵抗的区别，核苷类似物adefovir 和tenofovir与拉米夫定、elbivudine或者 entecavir不会产生交叉抗药性。Adefovir第一年治疗的抗药性几乎没有，但是在治疗的第四年末可以达到30%。而Adefovir在拉米夫定抵抗的乙肝患者的治疗中非常有效。但是以下因素限制了Adefovir的临床应用：它能最弱，抑制HBV DNA水平最慢，产生雪情转换的可能性最小，最容易导致原发无反应。

八成的HBeAg阳性口服抗病毒药物患者在血清转换后接受6到12个月或者更长的巩固 治疗可以获得一个长期的疗效

Consolidation treatment for 6 to 12 months or more after HBeAg seroconversion achieves a durable response in approximately 80% of HBeAg-positive patients who have received oral agents,^57,58,59 whereas all but a small minority of HBeAg-negative patients usually have a relapse after therapy.^31,60 Because responses are not always durable, careful post-treatment monitoring is required to identify relapse (especially rare, severe, and sometimes fatal post-treatment flares in patients with cirrhosis) and to reinstitute therapy. Thus, nearly all HBeAg-negative patients and approximately 80% of HBeAg-positive patients who do not undergo HBeAg seroconversion should continue nucleoside or nucleotide therapy after the first year; in the absence of resistance, such therapy generally maintains clinical effectiveness.^{39,40,45,61,62,63}

Successful antiviral therapy retards hepatic fibrosis,^{33,37,38,64,65} even reverses cirrhosis,^66,67 and improves survival.^68,69,70 Unlike pegylated interferon, oral agents are effective in patients who previously did not have a response to interferon,^{33,35,37,42,44} can be used safely and effectively as salvage therapy in patients with hepatic decompensation (delaying or averting liver transplantation),^71,72,73,74 and, in patients with advanced fibrosis and cirrhosis, may prevent hepatic decompensation.⁷⁵ Thus, the introduction of oral nucleoside and nucleotide analogues has been lifesaving in HBV infection, paralleling a 30% reduction (from 586 patients in 2000 to 406 patients in 2006) in the number of patients listed for liver transplantation annually in the United States.⁷⁶

The side effects of pegylated interferon include flulike symptoms, marrow suppression, depression and anxiety, and autoimmune disorders, especially autoimmune thyroiditis; close medical supervision and laboratory monitoring are required. Most oral agents have an acceptable side-effect profile even after extended use,^39,40,45,77 but because adefovir and tenofovir may cause nephrotoxic effects, periodic monitoring of renal function during nucleotide therapy is advisable.^39,40 In preclinical rodent-toxicology studies, doses of entecavir that were 30 to 40 times higher than those that were used in humans were associated with lung, brain, and liver tumors, which have not been observed in higher species (e.g., rabbits and dogs).^42,44,45 Telbivudine, too, appears to cause few major toxic side effects, although grade 3 and 4 elevations in levels of creatine kinase were more common in patients treated with telbivudine than in patients treated with lamivudine after 2 years of therapy,⁴⁸ and peripheral neuropathy has been attributed to telbivudine.

Treatment with pegylated interferon for 1 year is more likely to result in HBeAg seroconversion than is treatment with an oral agent for 1 year³⁰; however, oral agents are usually administered for more than 1 year and achieve similar rates of HBeAg seroconversion (approximately 30%) by the end of 2 years, approaching approximately 50% at 5 years.^45,49,61,63 Similarly, earlier studies suggested that rates of HBsAg seroconversion at 1 year are higher for interferon-based therapy than for oral agents.^26,30,31 However, rates of HBsAg loss are similar between pegylated interferon and some of the newer, more potent oral agents (Table 1 and Table 2).^45,51 In addition, after successful HBeAg seroconversion and cessation of therapy in Western (not Asian) patients, patients who have received lamivudine appear to have rates of HBsAg seroconversion (20% at 3 years in one small study) that are similar to those achieved after interferon therapy.^58,68,78,79 Reductions in cccDNA are similar in patients with spontaneous, interferon-induced, or oral-agent–induced HBeAg seroconversion.⁸⁰

Two other oral agents that appear to be efficacious against HBV but are not yet approved by the Food and Drug Administration are emtricitabine and clevudine. Emtricitabine, which is similar in structure, efficacy, and resistance profile to lamivudine,⁸¹ appears to confer no advantage over lamivudine. Clevudine is distinguished from other oral agents by its sustained suppression of HBV DNA for several months after cessation of therapy.^82,83,84 However, preliminary clinical trials suggest that clevudine is less potent than other oral agents in suppressing HBV DNA and inducing HBeAg seroconversion.^83,84

Resistance to Antiviral Drugs

Resistance does not appear to emerge during pegylated interferon therapy. L-nucleosides (e.g., lamivudine and telbivudine) are associated with the emergence of mutations in the YMDD motif (tyrosine, methionine, aspartate, aspartate) of HBV DNA polymerase domain C and with upstream compensatory mutations in polymerase domains A and B that, collectively, reduce treatment efficacy. The nucleotide analogues (adefovir and tenofovir) are associated with mutations in polymerase domains B and D. Although resistance to lamivudine is sufficiently high to limit its clinical impact, resistance to the cyclopentyl guanine analogue entecavir and tenofovir remains low (Table 1 and Table 2). Ultimately, drug resistance reduces drug effectiveness^66,75 and may precipitate hepatic decompensation in patients with advanced cirrhosis and after liver transplantation. In addition, because of cross-resistance between several of the oral agents, the emergence of resistance to one drug (e.g., lamivudine) eliminates the option for subsequent treatment with others (e.g., telbivudine and entecavir [see below]). Because of 1-to-2–year treatment-emergent resistance,⁴⁹ telbivudine has not been widely used for the treatment of chronic HBV infection. The nucleotides are effective in nucleoside resistance and vice versa.^54,55,85 Entecavir, at a dose of 1 mg, is approved for lamivudine-resistant HBV; however, entecavir resistance emerges in 7% of patients at the end of year 1, in 16% of patients at the end of year 2, in 35% of patients at the end of year 3, and in 43% of patients at the end of year 4.^86,87 Specialized assays are available to detect these mutations. However, the emergence of resistance can usually be detected by an increase in HBV DNA of greater than 1 log₁₀ after an initial virologic response (in the absence of nonadherence,⁸⁸ which accounts for breakthrough in 30% of patients treated in clinical trials⁵), especially when accompanied by an elevation in the ALT level. More detailed overviews of antiviral resistance in HBV infection appear elsewhere.^{6,89,90,91,92}

Predictors of Response

Factors that are most predictive of a response include a high ALT level, a low HBV DNA level, and mild-to-moderate histologic activity and stage.^93,94 The genotype is associated with higher frequencies of spontaneous (B>C)^19,95 and pegylated interferon alfa-2b–related (A>B>C>D) HBeAg and HBsAg seroconversion,^20,96 but it does not correlate with the degree of HBV DNA suppression associated with the oral agent.⁹⁷ In clinical trials of oral agents, numbers of events were too small to determine the influence of the genotype on HBeAg seroconversion. The rapidity and profundity of HBV DNA suppression during oral-agent therapy is predictive of the virologic, serologic, biochemical, and histologic benefit at the end of 1 year of therapy.^{5,48,52,98,99} Three oral agents have low genetic barriers to resistance — lamivudine, telbivudine, and, to a lesser degree, adefovir. In lamivudine and telbivudine, the level of residual HBV DNA at the end of the first half-year of therapy is inversely proportional to the frequency of drug resistance by the end of the year of therapy. In adefovir, the level of residual DNA at the end of a full year is inversely proportional to the frequency of drug resistance by the end of the second year. Other factors favoring resistance to lamivudine, telbivudine, and adefovir include high baseline HBV DNA and treatment of long duration.^{6,89,90,91,92}

Combination Therapy

Combinations of available antiviral drugs for HBV infection in patients who have not received treatment do not increase efficacy. Although combinations of pegylated interferon and lamivudine yielded a reduction in HBV DNA of an extra 1 to 2 log₁₀ during therapy, the combination did not result in a durable post-therapy benefit.^30,31 Similarly, telbivudine and lamivudine combined did not achieve additional antiviral activity over that of telbivudine alone.⁴⁷ Combination therapy with agents of differing resistance profiles should limit the emergence of resistance; however, resistance is so negligible during the early years of treatment with entecavir or tenofovir that demonstrating the superiority of preemptive combination therapy over initial monotherapy will be challenging. Indeed, adding a second, complementary drug after the emergence of resistance has been a very successful strategy.^54,55,100 Because of the lack of data to provide support for the efficacy of combination therapy over monotherapy in patients who have not received treatment, current treatment guidelines⁵ do not recommend combination therapy except for patients in whom drug resistance can precipitate or aggravate hepatic failure, as in decompensated cirrhosis or after liver transplantation. Among patients with drug-resistant HBV who have received treatment, available data provide support for adding, rather than switching to, a second drug with a different resistance profile.^5,6,100

HIV and HBV Coinfection

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Fitness topic: A Personal View on Recreational Therapy of Massage

“Recreational therapy, also referred to as recreation therapy and therapeutic recreation, contributes to the broad spectrum of health care through treatment, education, and the provision of adapted recreational opportunities — all of which aid in improving and maintaining physical, cognitive, emotional, and social functioning, preventing secondary health conditions, enhancing independent living skills and overall quality of life.”, cited from wikipedia encyclopedia. As you can see, it is a topic with a broad spectrum; so definitely, I am not going to talk all about it. In this article, I am going to cover some of the fundamental issues highlighted in sports medicine. However, if you are a sports medicine practitioner, then this article probably will be just a review of your knowledge except some of my personal opinions and that knowledge belong to the TCM field.

      Currently, I am serving as a massage therapist in the Olympic Village, of course, like many of my schoolmates; it is a volunteer position other than paid position. And no doubt that is why we can ourselves volunteers, and we serve the athletes and coaches as well as officials who live in this village with both our heart and soul. Once again, even with a strong devoted mind, it doesn’t seem enough. Without the professional knowledge backup, how would a satisfactory massage/medical service come out? So it let me think again what proficiencies should a massager have got?

     For a real traditional Chinese medicine type massager, probably, he or she doesn’t need to know modern anatomy, because our ancestors rarely know what the human body is made of (leave the qi, blood, essence and fluid alone). But for a modern Chinese massager, no matter your knowledge is TCM-based or modern science-based, you have to know the anatomy and some of the important issues like special tests in the orthopedics field. For the former issue, it can get you a clear idea for what you are doing or which part of the human body you are working on; whereas for the later issue, it really perfect your practice either as a orthopedists or massager or other medical practitioners, for it can elucidate the diagnosis and let you know what is wrong with this patient even though on most occasions nowadays, customers who go into your practicing room with the only wish of body relaxation. Given the TCM has no anatomy, some of you may claim it does have, but here I do not want to argue on this issue, because if it does have anatomy, this anatomy is not we talk nowadays (think about the five zang organs), how can it come up with a modern diagnosis? Also, some of you may claim, TCM does have a clear diagnosis, what I want to say, yes, it does, but this diagnosis is not what we commonly talk today and all lay people including most of our modern Chinese people, do not know what we are talking about. With only a TCM diagnosis, it is impossible for us to communicate with other medical professional from a different medical background. And then, it is impossible for the patients get the best medical service. Luckily, as time changes, things change, students in the TCM field change, and probably you have noticed that the name of diseases in some of our TCM textbooks begin to change, they are just getting more and more western medicine-styled.

      So, that is why, like lots of TCM practitioners nowadays, I highly approve of a conventional diagnosis plus TCM treatment. It makes things easier and much clearer and makes the motto “patients deserve the best medical service” possible to come true. Then, problems arrive, besides a kind fully devoted heart, how can we get there on the academic level？Here, I am going to take massage for an example, and hope you can get some new ideas for your practice.

I am a novice or intern, so, propositional to my current status, the knowledge or topic here will mainly be intern-level. One more thing, I am going to point out is, I am not going to cover the TCM part considering our university is the best one and my schoolmates are quite professional on that, and perhaps lots are better than me.

    Anatomy review: for a massager or a sports medicine related staff, I think it is of great significance to know the anatomy of the musculoskeletal part. The spine is the very important part; you have to know the morphological characters of every vertebra (cervical, thoracic, lumbar, sacrum, coccyx) and intervetebral disc, ligaments (ALL, PLL, ligamentum nuchae, interspinal/intertransverse). Knowledge of muscles including those deep small back muscles is a crucial prerequisite for your practice. If you know all the origination, insertion, innervation and function, a new world will be open for you.

     On the back, the erector spinae is the most important one, it arises by a broad tendon from posterior part of iliac crest, posterior surface of sacrum, sacraoiliac ligaments, sacral and inferior lumbar spinous process process and supraspinous ligaments. It branches into iliocostalis which inserts to luborum, thoracis, cervicis, longissimus which inserts to ribs between tubercles and angles to transverse processes in thoracic and cervical regions and mastoid process of the temporal bone, spinalis which inserts to more superiorly positioned spinous processes.

     Deep layer muscles include semispinalis which arises from transverse processes of C4-T12 vertebrae and inserts to spinous process of more superior vertebrae; multifidus which arises from posterior sacrum, posterior superior iliac spine of ilum, aponeurosis of erector spinae, sacroilia ligaments, mammillary processes of lumbar vertebrae, transverse processes of T1-T3, articular processes of C4-C7; rotatores which arises from transverses processes of vertebrae and inserts to junction of lamina and transverse process or spinous processes.

       Minor deep layer muscles include interspinalis, intertransversarii, levatores costarum (they arise from tips of transverse processes of C7-T11 vertebrae and pass inferolaterally and insert on ribs between tubercle and angle)

      Others are universally known ones which include serratus posterior superior and inferior, spenius (arises from nuchal ligament and spinous processes of C7 –T3 or T4 vertebrae and one bundle named splenius capitis inserts to mastoid process and lateral third of superior nuchal line of occipital bone, the other named splenius cervicis which inserts to tubercles of transverse processes of C1-C3 or C4 vertebrae)

     Deep extrinsic shoulder muscles and superficial ones are all universally known ones. They include levator scapulae, rhomboid major and minor, trapizius, latissimus dorsi.

      Scapulohumeral muscles include deltoid, suprapinatus, infraspinatus, teres major and minor, subscapularis. All these muscles are quite easy to remember.

     Muscles around the arm: biceps brachii, brachialis, coracobrachialis. Extensors: triceps brachii, anconeus (lateral epicondyle to lateral surface of olecranon and superior part of posterior surface of posterior surface of ulna). For the anconeus, besides as an extensor muscle, it also pulls the capsule around the olecranoan of the ulna and humerus away preventing capsule impingement.

      Muscles of the forearm: flexors: pronator teres, flexor carpi radialis, palmaris longus, flexor carpi ulnaris, flexor digitorum superficiali and profundus, flexor pollicis longus, pronator quadratus…..

Diagnosis: usually, besides chest x ray, blood analysis and other biochemical tests, one important part of modern sports medicine that elucidate the diagnosis is Special Tests. With these tests, you can probably know much of your patient’s physical status and your treatment will be more focused. The following part is those tests used quite often in the modern sports medicine field. Note that not all these tests are one hundred percent sure for the diagnosis, and you have to know the specificity and sensitivity of the test in order to have a better idea what the result of the test means to the patient.

Comparison of medical student training in the US and  our university

As a medical student in BUCM, we usually spend seven years medical school education before we take the medical licensing examination to become a physician. However, as you may know that in the US, it usually takes four years medical school plus four years undergraduate education, totally eight years for students to get an M.D. certificate and take USMLE. Kind of shortcut to success, here in our university, we usually spend totally seven years or even five years to become a M.D. equivalent and be qualified to take the medical licensing examination and become a physician. However, in fact, if we leave the traditional Chinese medicine alone, no matter in the knowledge level or practice level, we, as a graduate from BUCM, can never compete with those graduates from medical school in the US. I have been pondering this for a long time, and it seems that we can not find a way to get more superior than most of the conventional medical students in China, let alone those US medical graduates. How can we survive this cruel world full of competitions? Students who graduate from BUCM, most of them can not be matched to relative good hospitals in China with comparison with conventional medical school graduates in China of the same level. What can we do? Theoretically speaking, we know much more than those graduates from conventional medical schools, and we should have better and more opportunities than them. But currently the fact is totally the contrary. The opportunities and the payment that the employer, the hospitals in China can offer us TCM students, compared to graduates from conventional medical schools of the same level, are much less. Frankly speaking, that is not proportionate to the work  we have done in BUCM. We spend four and a half years medical course learning at the school and hospital, learning Chinese medicine, western (conventional) medicine, biological courses or even some rehabilitation courses at the same time within this relatively short period of time; and we, like most of the readers here, also have or will have spend two and a half years in clinical settings learning and practicing both traditional Chinese medicine and conventional medicine. So , definitely we, as students from BUCM spend more time and energy working on this career, and to a certain extent, if we really learn and practice, we can be more competent in the fiercely-competing job market, and we can, of course, be better doctors than those who just know the one medical system. So, in that ideal situation, definitely, we will have more chances to be recruited into famous and good hospitals with good payments. For as you may notice, that in many cases, especially for cancer patients requiring chemotherapy, females with menstrual problems, and most patients in the neurology department, or in the pediatrics department, the effects of conventional therapies are quite limited. That’s where we, as an integrative medicine practitioner, can light the hope to our patients.

However, that is the ideal or kind of dreaming situation; nowadays, we do not have that social status, we are kind of lower than those western doctors in the food chain (this word may be not appropriate). And even in China, the fist idea when folks get sick is running into a western hospital other than TCM hospital even in some cases, TCM is their best choice, like those I mentioned in the last paragraph. Why, why patients prefer western medicine than Chinese medicine? Why, why do we earn much less than those western medicine practitioners? Once again, recall what you have done when you are in this TCM university, what you have done during you internship years. I think no doubt; you will come up with an answer.

Then, my question here is not why plus a questioning mark any more, my question is how, how to change this situation? Given the US has the best medical education, given the US doctors earn quite a lot and are among the best respected group of people in the world, we should learn something from their medical education and physician training.

Probably you have read the article in my website which is cited from the survival guide for the 3^rd and 4^th year’s medical students in the US, and something you have to admit and accept, but at the same time, those are most of the things you can not change because of different education systems.However, we can do something to get better prepared and better improved and better competent as we are having internships in the hospital. Then, how to do it? Do some comparisons between us TCM interns in the ward with the ward personnel in the US, find the corresponding level and get qualified as that level of medical student in the US requires. For example, comparably speaking, I am as a fifth or sixth grade medical student in BUCM, and I am taking my internship in Guanganmen Hospital, so, I should be kind of the intern level student in the American ward, so what I should and have to get qualified is to be responsible for the moment -to-moment patient care, be paired with an intern who will work with me on the patients i am assigned and it lies the same for all other things of this intern level.

More things should be done; more knowledge should be grasped, for me and for you as a TCM student in BUCM. No matter whom you are, what grade are you in, I think you can find a relative level in the US medical education system and get prepared as this system requires for western medicine practice. So I think, in the near future, we can change the world’s opinion about TCM doctors. One more issue, be strong-minded, unless you can not pursue the happiness of integrative medicine

something elese we can do:

Remember that there is a person on the other end.

Enthusiasm.

Assertiveness.

Reading.

Have a good time.

Respect your fellow classmates.

Be friendly with support staff, especially the nurses.

Be on time.

Ask questions.

Seek feedback .

Let your intern/resident know where you are at all times .

Work hard.

Take initiative.

Know your patients better than anyone else.

Appropriate humility.

Understand responsibilities and expectations.

Be prepared to be on -call the first night .

Appearance and demeanor are important.

Prepare/practice for oral presentations.

Efficiency is key.

Remember Patient Confidentiality.

aha. anyway, you have the rights to dispise me for this opinion and i respect you on that level.

嘿嘿,你享有鄙视的权利. (自勉文章，谢谢赏析)

                          THE WARD TEAM
The members of the team are described below. Students are an integral member and may be most knowledgeable about a patient.

Attending Physician has completed a residency and possibly a fellowship and is a member of the Northwestern faculty. He or she is ultimately responsible for the patient's care and will thus make or approve all major decisions. A private patient will have a private attending. A clinic patient will have a floor or service attending assigned for coverage. If they have both, the floor attending has the teaching responsibilities, while the private attending has the patient management responsibilities.

Fellow has completed a residency program and is now in subspecialty training, e.g. cardiology, vascular surgery, high -risk obstetrics, etc. As a junior student, your contact with these individuals will occur in the setting of a subspecialty consult. Fellows are, in general, exceptionally knowledgeable about their specialty, and as such, are excellent teachers.

Resident is anyone with more than one year of postgraduate training.Since attendings typically round once a day, the resident is in charge of the team. Besides helping the intern in managing the team's patients, he or she is also primarily responsible for the education of students. Clerkship evaluations are usually solicited from residents.

Intern is anyone in the first year of postgraduate training (PGY-1). The intern is primarily responsible for the moment -to-moment patient care. You may be paired with an intern who will work with you on the patients you are assigned. The intern usually has many tasks to be
completed through the day, so any work you can do to help out will be greatly appreciated. In return, they can show you the ropes around the hospital and offer a good evaluation of your performance to the resident.

Senior Student is a fourth year medical student who is taking an elective or a sub-internship (Sub-I). He or she has the responsibilities of an intern and is supervised by the resident.

Junior Student: The goal of the junior clerkships is to continue to teach you the clinical skills of a physician. During the M1 and M2 years, you learned pathophysiology, problem solving, and patient interaction skills. During the ward years you will learn how to integrate and apply
these skills towards actual patient care. This is a challenging endeavor, but you will slowly improve as the year progresses.

  You or we will frequently find that you lack knowledge of a particular disease process or the skills to perform a certain procedure. Remember, you are there are to learn, and nobody expects you to know everything already. In time, your clinical judgment problem solving skills, ability to manage patient issues, and self-confidence will
develop.

Medical Videos on Sale：

 本人有若干全英文临床和基础医学视频CD出售,详情请进本人主页,并和本人联系

CD Names and Prices

CD 名称和 价格

1.       Patient Care Skills    30RMB

介绍：本CD共286 MB，主要讲授临床最基本的操作，包括Body Mechanics，Gloving，Turning and Position, Transfers, Range of Motion, etc.

2.       Medical Immunology  50RMB

介绍：2个CD共851 MB，是美国著名医学院免疫学的讲课全程录像，内容包括医学免疫学的所有内容。

3.       Medical Microbiology  60RMB

介绍：2个CD共1.06GB，是美国著名医学院医学微生物学的讲课全程录像，内容包括细菌学，立克次体和病毒学的所有内容，包括临床病例分析。

4.       Clinical Procedures  50 RMB

介绍：2个CD共802 M