1、臨床科研論文的撰寫 周卸來杭州師范學(xué)院臨床醫(yī)學(xué)院 論文類型論著(Original Article)論著摘要(Abstract of Original Article )臨床診治經(jīng)驗介紹(Clinical Experience)病例報道(Case Report)簡報(Brief Report)綜述(Review)選題-選題原則創(chuàng)新性先進(jìn)性科學(xué)性可行性選題-選題方法從各學(xué)科領(lǐng)域的研究前沿選題：大單位、大課題, 如863、973課題、國家自然科學(xué)基金重大課題等。從自己的實際工作過程中發(fā)現(xiàn)問題，并且此問題是可以通過科研來加以解決的。通過閱讀文獻(xiàn)，綜合文獻(xiàn)資料，來找出適合本人的課題。論著的基本內(nèi)容文題作

2、者及單位中英文摘要及關(guān)鍵詞引言資料(材料)與方法結(jié)果討論參考文獻(xiàn)摘要目的 分析腦動靜脈畸形(AVM)患者的臨床特征并評價其手術(shù)治療的療效。 方法 收集1956年1月2001年10月間本院收治的2086例腦AVM患者的臨床資料, 對其年齡、性別、Spetzler-Martin分級、首發(fā)癥狀進(jìn)行分析。對1992年后行顯微外科切除的635例患者，按入院時間先后分成1992年1996年和1997年2001年兩組，再比較兩組間的Spetzler-Martin分級和手術(shù)并發(fā)癥發(fā)生情況。結(jié)果 本組病例腦AVM好發(fā)年齡2040歲，首發(fā)癥狀最常見的是腦出血(43.4%)、頭痛(24.9%)、癲癇發(fā)作(17.3%

3、)，Spetzler-Martin分級、級患者的構(gòu)成比分別為。1992年1996年組和1997年2001年組之間比較，Spetzler-Martin、級患者的比例顯著下降(P)，級顯著升高(P)，主要術(shù)后并發(fā)癥的發(fā)生率（死亡、偏癱、顱神經(jīng)功能障礙和胃腸功能出血）無顯著性差異(P=0.796)。結(jié)論Ultrastructural Changes of penile Tunica Albuginea in Diabetic RatsYing-li LU1, Xie-lai ZHOU2, Zhou-jun SHEN2, Hua WANG2, Shan-wen CHEN2, Zhao-dian CHE

4、N21Department of Endocrinology, Sir Run Run Shaw Hospital, 2Department of Urology, First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou 310016, ChinaKeywords: tunica albuginea; penis; diabetes mellitus; scanning electron microscopyAbstract Aim: To clarify the ultrastructural

5、changes of penile tunica albuginea(TA) in streptozotocin (STZ)-induced diabetic rats. Methods: Intraperitoneal injection of STZ was used to induce diabetes mellitus(DM) and twelve successfully-induced Sprague-Dawley rats were collected for the diabetic group. Another ten age and weight-matched rats

6、were used for control group. Blood samples from the tail snips of the rats were used for determination of serum glucose levels with SureStep Plus Blood Meter. At four and ten weeks after the injection, half of the rats in each group(n=6 in diabetic group, n=5 in control group) were killed and penile

7、 samples were obtained from middle point of the whole length of penile shaft for examination of TA under scanning electron microscopy. Results: In the diabetic group, the serum glucose levels were higher(P=0.005 and P=0.003 at 4- and 10-week time points, respectively) and the TA were thinner(P=0.012

8、 and P=0.019 at 4- and 10-week time points, respectively) than those of control group. In the control group, the fibers of TA were rich and arranged regularly and undulatedly, while in the diabetic group, the fibers diminished, lost the undulations and arranged irregularly. Conclusion: In rats, DM w

9、ould impair the ultrastructures of penile TA, and this impairment could contribute to diabetic ED in part by impairing the veno-occlusive function.1 IntroductionChronic complications of diabetes mellitus(DM) are a much larger burden on both diabetic patients and overall medical costs than diabetes i

10、tself. Erectile dysfunction (ED) is very common among diabetic patients. Men with diabetes are afflicted with ED at a much higher incidence and an earlier age than normal men，with a consequent reduction in quality of life1. An investigation from Hong Kong demonstrated that the prevalence of ED in di

11、abetic male patients was 63.6%, which was significantly higher than that of undiabetic men2. A study from Italy show that the incidences of ED of Type 1 and Type 2 diabetic men aged 20-61 years were 51% and 37%, respectively. Both of the prevalence and severity of ED increased with age for both type

12、s3. ED in diabetes seemed to result from combinations of impairments from nearly every step in the production of a penile erection. Simopoulos et al4 studied the corporeal structural and vascular micro-architecture in diabetic rabbits with X-ray micro computerized tomography. The study results showe

13、d that in diabetic rabbit penises, there existed a significant decrease in corporeal vascular volume and cavernous artery diameter when compared to normal controls. Burchardt et al5 investigated the endothelial and smooth muscle density in the corpora cavernosa of the STZ-induced diabetic rat and fo

14、und that the density was significantly decreased in diabetic corpus cavernous but not in normal age-matched rats. Salama et al6 evaluated the ultra-structural changes of penile TA in diabetic rats under scanning electron microscopy and the results demonstrated that, with progress of the DM, an incre

15、ase in both thickness and loss of undulation of collagen bundles in penile TA was appreciated. Italiano et al7 investigated the structural changes of penile cavernous and dorsal nerves in streptozotocin-induced diabetic rats, and disclosed a significant decrease of myelinated fibre size, diffuse acc

16、umulation of glycogen within axons, lipid droplets in Schwann cells and pronounced sequestration of axoplasm by adaxonal Schwann cell processes. Nitric oxide (NO) is a physiologic signal essential to penile erection, and disorders that reduce NO synthesis or release in the erectile tissue are common

17、ly associated with erectile dysfunction. NO synthase(NOS) catalyzes production of NO from L-arginine. While both constitutively expressed neuronal NOS (nNOS) and endothelial NOS (eNOS) isoforms mediate penile erection, nNOS is widely perceived to predominate in this role. Demonstration that blood-fl

18、ow-dependent generation of NO involves phosphorylative activation of penile eNOS challenges conventional understanding of NO-dependent erectile mechanisms. Regulation of erectile function may not be mediated exclusively by neurally derived NO. nNOS may initiate cavernosal tissue relaxation, while ac

19、tivated eNOS may facilitate attainment and maintenance of full erection8. Bloch W et al9 examined the existence and location of the eNOS in penile specimens, and found a distinct expression of eNOS in the cavernosal smooth muscle, large quantities of eNOS in the small intracavernosal helicine arteri

20、es. The result indicated eNOS as a main source of NO alongside nNOS, and also an important role in vascular regulation. Akingba AG et al10 explored the possible relevance of eNOS in the pathophysiology of diabetic ED in the penis of alloxan-induced diabetic rats. The results showed that in the penis

21、 of the diabetic rat, eNOS protein expression and synthetic activity were reduced compared with the normal rat penis, independent of testosterone influence and in the absence of significant erectile tissue degenerative changes. These eNOS effects apparently preceded nNOS effects. El-Sakka et al11 st

22、udied the changes of nitric oxide synthase(NOS) in diabetic rats and concluded that, in the diabetic group, there was a significant decrease in NOS containing nerve fibers in the dorsal and intracavernosal nerves, down-regulation of nNOS and iNOS mRNA expression, down-regulation of nNOS protein expr

23、ession, and less nNOS-positive immunostaining in the dorsal and intracavernous nerves.All above study results suggest that the DM can not only destroy the erectile structures, but also interfere in the balance of erectile neurotransmitters, and thereby induce the diabetic ED.The tunica albuginea(TA)

24、 is a fibroelastic sheath surrounding the trabecular smooth muscle of the corpus cavernosum and is composed mainly of thick collagen bundles and elastic fibers12. The collagen and elastic fibers are the key structures of the penile compliant tissue that permits the increase in girth and length of pe

25、nis during tumescence, while provides adequate resilience to return rapidly to the flaccid state during detumescence13. In the literature, there are few reports on the morphological alterations of TA in diabetes, and if the TA involves in the courses of DM inducing ED is still unclear. The present i

26、nvestigation is designed to clarify the ultrastructural changes in penile TA in streptozotocin (STZ)-induced diabetic rats.字，篇參考文獻(xiàn)引言應(yīng)強(qiáng)調(diào)大宗病例的意義；治療手段的發(fā)展方向和選擇依據(jù)。材料或資料 材料要注明廠家、批號、型號等，病例資料包括一般內(nèi)容及與本文有關(guān)的特殊內(nèi)容(有的特殊內(nèi)容視情況要放到結(jié)果中去寫)。特別在病例的選擇和分組上應(yīng)交代清楚。 應(yīng)注明病例的納入標(biāo)準(zhǔn)方法 包括分組、被試因素、評價指標(biāo)、指標(biāo)的測定方法及統(tǒng)計學(xué)處理方法等，有時可引用相應(yīng)的參考文獻(xiàn)來省去方

27、法學(xué)敘述。 樣本量的估計 a.憑經(jīng)驗：在動物實驗中，分為大動物（犬、豬）、中等動物（兔、豚鼠）、小動物（大鼠、小鼠），每組分別為515、1020、1530；難治的疾病，療效顯著時（如惡性腫瘤）510例即可；急重病死亡率高的（如休克、心衰、腎衰、呼吸衰竭）需3050例；一般病和慢性病100500例；多因素分析中樣本含量數(shù)至少是研究因素個數(shù)的510倍以上。 b.計算法統(tǒng)計學(xué)處理常用統(tǒng)計方法：t檢驗、卡方檢驗、方差分析、非參數(shù)檢驗。統(tǒng)計軟件：SPSS、SAS等。 隨訪成功率、失訪率一定要注明，第二句話表述模糊不清應(yīng)標(biāo)明使用什么統(tǒng)計軟件。分組應(yīng)另起一段，為什么要這樣分組要交代清楚。兩組間除了干預(yù)因素不

28、同外，應(yīng)具有可比性。結(jié)果 可按具體情況用文字、圖、表來敘述，但不能累述。數(shù)據(jù)資料應(yīng)做統(tǒng)計學(xué)處理，給出統(tǒng)計量。最好分小節(jié)來寫, 每小節(jié)寫一項結(jié)果。結(jié)果部分是學(xué)術(shù)論文的關(guān)鍵所在，應(yīng)占較大的篇幅。分段寫，套用固定格式。兩組間的Spetzler-Martin分級比較結(jié)果應(yīng)有統(tǒng)計學(xué)依據(jù)。表1 各組內(nèi)實驗組和對照組間腹膜粘連程度的比較組別對照組(n=12)實驗組(n=12)HP00A組23050.054周27300660004.4590.05B組2周01146002370.1470.054周001290001111.2400.05C組2周05520282006.7430.054周

29、25410561003.6760.05結(jié)果書寫常用的格式 2.2 腹膜粘連程度比較 見表1, 表中結(jié)果顯示：創(chuàng)傷致粘連組（A組）和結(jié)扎血管致粘連組（C組）中，無論是術(shù)后2周還是術(shù)后4周，實驗組的粘連程度均顯著低于對照組（P0.05)；而滑石粉致粘連組（B組）術(shù)后2周及4周的粘連程度，實驗組和對照組間均無顯著性差異（P0.05）。說明殼聚糖凝膠對創(chuàng)傷及缺血所致的腹膜粘連有明顯的預(yù)防作用，而對滑石粉所致的腹膜粘連則作用不明顯。 討論 應(yīng)緊密結(jié)合本人的結(jié)果，適當(dāng)引用參考文獻(xiàn)而展開。主要是對本人的結(jié)果進(jìn)行分析討論，有時也可對文中獨創(chuàng)性的設(shè)計或方法進(jìn)行討論。討論中應(yīng)注意的問題不用第一人稱，要用第三人稱。不能漫無邊際或面面具到，而應(yīng)該重點突出。不盲目夸大本人結(jié)果的意義、價值。條理要清楚，邏輯性要強(qiáng)。一般不用文學(xué)性詞匯。討論中常套用的格式1 提出問題：以標(biāo)題的形式或在段落開頭以一句話提出。2 交代現(xiàn)狀：為下文作鋪墊，一兩句話即可。3 引用文獻(xiàn)：可以作者、國家、年份等開頭做引用，注意文獻(xiàn)序號標(biāo)注的不同。4 闡述自己的結(jié)果：注意不要照抄結(jié)果部分的內(nèi)容，而應(yīng)有所取舍，高度概括。5 分析討論：自己結(jié)果與文獻(xiàn)的異同點，分析其中的原因、機(jī)制等，最后得出結(jié)論。引用參考文獻(xiàn)引用參考文獻(xiàn)應(yīng)適當(dāng)分析原因不能用第一人稱表述比較模糊摘要 目的、 方法、 結(jié)果、 結(jié)論(由結(jié)果推出的結(jié)論) 摘要