Objective The hardcore of Chinese general practice residency (GPR) program is diagnosis and treatment. The training of specific clinical skills is scant. As aging population is on growth, chronic disease management should been shed more lights on. For such reason, this article aims to elaborate the clinical skill training for GPR with the case of adult weigh management (AWM). Methods and Results Referring to the Obesity Guidelines for Clinicians, the authors raise up three approaches to address the issue. Namely, (1) enhancing the sensitivity to obesity and overweight; (2) improving the ability to diagnose obesity and overweight; (3) integrating ABCDEF strategy into syllabus and constructing a mentor demonstration-mentee practice-feedback loop in training. Conclusions Although the applicability of clinical training of AWM has still been tested, the implementation of it will definitely inspire future general practice physician who plays a major role as community’s health gate keeper. Key words: General practice residency; Obesity; Weight management; Clinic teaching

溃疡性结肠炎(Ulcerative colitis,UC)是主要累及结直肠的慢性非特异性疾病[1],NK/T细胞淋巴瘤为非霍奇金淋巴瘤(non-hodgkin lymphoma,NHL)少见类型,占NHL的5％～15％[2].

造血干细胞移植(hematopoietic stem cell transplantation,HSCT)是急性髓系白血病有效的治疗手段之一,但移植后复发率高,多于1 年内出现,是移植失败的主要原因之一,目前尚无标准有效的治疗手段.本文报道1 例急性髓系白血病于移植后6 年髓外多部位复发,从髓外复发危险因素及发病机制进行讨论,希望能提高临床医师对移植后髓外复发的了解.

1 病例资料 患者女,32岁,因“反复腰痛伴头晕、乏力2月余”于2015年4月20日人院.患者入院前2个月无明显诱因出现腰痛、乏力,双下肢麻木,凌晨及夜间加重,面色呈进行性苍白,伴活动后胸闷、气促,碰撞后皮肤易出现瘀斑,无鼻衄,无牙龈出血,无月经量增多.查体:体温(T)36.6℃,脉搏(P)76次/min,呼吸(R)20次/min,血压(BP)98/58 mmHg,中度贫血貌,全身皮肤、黏膜无黄染,无皮下出血点及瘀斑.全身未触及浅表淋巴结肿大;双肺呼吸音清,未闻及干湿哕音;心界无扩大,律齐,心音有力,各瓣膜昕诊区未闻及病理性杂音.肝脾肋下未触及,肝区肾区无叩击痛;双下肢无水肿;脊柱前屈侧屈均受限.骨盆挤压试验(-),左侧4字试验(+),右侧4字试验(-),双侧直腿抬高试验(-).血常规:HGB:79 g/L、PLT:58×109/L、WBC:1.04×109/L.

异基因造血干细胞移植(allogeneic hematopoietic stem cell transplantation,Allo-HSCT)是血液恶性肿瘤最有效的治疗方法之一,可望达长期缓解并可能治愈.但移植后复发仍然是移植失败最主要的原因之一,主要为骨髓内复发,髓外复发(extramedullary relapse,EMR)发生率为0.65％～20％ [1-2].粒细胞肉瘤(granulocytic sarcoma,GS)是一种由髓系细胞来源的髓外发生的实体瘤.1988年Davey提出了髓外髓系肿瘤(extramedullary myeloid tumor,EMT)的概念,其中包括孤立性GS (非白血病性GS)和白血病髓外浸润(白血病性GS).白血病髓外复发多见于中枢神经系统及睾丸,以GS为表现的极为少见.

患者男,78岁,因"发现左颈肿物进行性增大1年"于2015年9月23日入院.1年前患者发现左颈部鹌鹑蛋大小肿物,逐渐增大,2015年9月16日CT:左侧颈中下部占位,考虑淋巴瘤.查体:左颈部扪及约3 cm×4 cm肿物,质韧,无压痛,触之无活动.双下肢中度水肿,余查体无异常.

再生障碍性贫血-阵发性睡眠性血红蛋白尿综合征(AA-PNH综合征)是一种多能造血干细胞疾病,既有一系或多系血细胞减少,又有溶血表现,病情较为凶险.目前,骨髓间充质干细胞(BMSCs)已广泛用于血液病的治疗,对于耐药且近期无法行异基因造血干细胞移植(allo-HSCT)的难治性患者是有效的治疗手段之一.

患者男，74岁，因“确诊真性红细胞增多症7年，白细胞升高1个月”于2013年11月1日入院。2006年出现全身皮肤呈暗红色，伴头晕，后因突发胸痛至河南某医院检查示红细胞（RBC）、血红蛋白（HB）升高（不详），诊断“真性红细胞增多症，急性心肌梗死”，予溶栓、口服羟基脲治疗，RBC、HB 控制正常。2013年10月19日复查血常规：WBC 12．5×109／L、幼稚粒细胞0．09、RBC 1．8×1012／L、HB 71 g／L。骨髓免疫分型：异常细胞占全部细胞的35．37％，表达 CD13，CD33，CD34，CD117，CD38， HLA－DR，CD7，MPO，cCD3（－），符合急性髓系白血病。染色体核型正常。入院查体：中度贫血貌，皮肤、黏膜无黄染，无皮下出血点及淤斑，无浅表淋巴结肿大，无胸骨压痛，心肺无异常，肝脾肋下可触及。11月3日查血常规：WBC 16．85×109／L、原幼稚细胞0．48、晚幼粒细胞0．05、HB 82 g／L、血小板（PLT）161×109／L。铁蛋白377．59 ng／mL。11月6日血涂片：中性中幼粒细胞0．02、晚幼粒细胞0．03、单核细胞0．17、原单细胞0．07、幼单细胞0．15；成熟红细胞大小不一，可见泪滴形及脊形红细胞。彩超：肝脾大，胆囊多发性结石，胆囊炎。家属拒绝骨髓穿刺及正规化疗。诊断：急性髓系白血病，予羟基脲、营养支持治疗，出院。

1 病例资料 患儿男,4岁11个月,因"多饮多尿,消瘦4月余"于2013年11月13日收入我院治疗.患儿2013年8月无明显诱因出现口渴,多饮多尿,每日饮水量4 000 mL左右,尿量每日约4000 mL,尿色清亮;伴消瘦,体重下降7 kg左右;常烦躁、哭闹、纳差.于当地医院行头颅MRI检查示垂体柄占位性病变(未见报告单).2013年11月23日入住我院神经外科治疗,查体示右眼眼球突出;全身浅表淋巴结未触及;双肺呼吸音清,未闻及干湿性哕音;心律齐,各瓣膜区未闻及病理性杂音;腹软,肝脾肋下未触及;神经病理征阴性.

Objective To investigate the protective effects on the renal allografts from brain dead (BD) donor rats pretreated with bone marrow mesenchymal stem cells (MSCs).Method Three groups [normal transplant group (G1).BD transplant group (G2),and MSCs pretreated + BD transplant group (G3)] were set up.Male F344 rats served as donors and male Lewis rats as recipients.In G1,kidneys from F344 donor rats were implanted into Lewis recipients.In G2,kidneys from F344 BD donor rats were engrafted into Lewis recipients.In G3,after BD was established in F344 rats,MSCs were given intravenously to the rats.The kidneys harvested 6 h later were transplanted to Lewis recipients.Cyclosporine was intromuscularly given daily to the recipient rats for 10 days.Right kidneys were resected from recipients on day 10.Creatinine level was examined on day 14,21,28,and 35.Renal allografts harvested on day 35 were pathologically detected.The irnmunochemistry expression of interleukin (IL)-1β and tumor necrotic factor (TNF)-α in renal allograft tissue was tested.Result Serum creatinine levels in G2 were remarkably higher than those in G1 and G3 (P＜0.01) on day 14,21,28,and 35 postoperatively.The creatinine levels on the above mentioned time points had no statistically significant difference between G3 and G1 except on day 21.Postoperative pathological changes in G2 of both pronounced infiltration of mononuclear cells and tubular epithelia[inflammation were notably increased in renal allografts as compared with those in G1 and G3.There was no obvious difference between G1 and G3 in infiltrated mononuclear cells and tubular epithelial inflammation.Positive expression levels of both IL-1β and TNF-α in glomerular,tubular and interstitial epithelial cells were statistically enhanced in G2 as compared with those in G1 and G3 (H =7.210,P =0.027),while there was no statistically significant difference in the expression of both IL-1[β and TNF-α between G1 and G3.Conclusion Brain dead donor rats pretreated with bone marrow MSCs might reduce renal allograft injury via decreasing both inflammatory cell infiltration and IL-1β and TNF-α expression.

目的 探讨尼古丁对脐带间充质干细胞(MSCs)形态学、细胞周期、细胞增殖及凋亡的影响.方法 不同浓度尼古丁作用于MSCs,以相差显微镜及原子力显微镜(Atomic Force Microscope,AFM)观察形态学变化;MTT法分别于24h、48h、72h检测细胞增殖;流式细胞仪法于24 h检测细胞周期与细胞凋亡.结果 尼古丁作用于MSCs后,细胞固缩,细胞膜表面形成空洞及凹陷,微绒毛样突起多见;细胞周期改变,G0/G1期的细胞比例明显增加(P＜0.05),G2期及S期细胞比例则逐渐减少(P＜0.01),周期阻滞随着尼古丁浓度递增而增加;细胞增殖受抑,呈时间剂量依赖性,凋亡率增高,0.5、1、1.5mg/mL的尼古丁作用MSCs 24h后,细胞凋亡率均高于对照组.0.5mg/mL组凋亡率(4.867±0.404)％与对照组(3.300±0.400)％比较,差异无统计学意义(P＞0.05);1mg/mL组凋亡率(10.333±0.961)％、1.5mg/mL组凋亡率(44.367±3.612)％与对照组比较,差异均有统计学意义(P＜0.01).结论 尼古丁使MSCs形态及超微结构发生早期凋亡改变,阻滞细胞周期,抑制细胞增殖且促进其凋亡.

AIM: To explore the effects of nicotine on surface morphology,ultrastructure,proliferation,cell cycle and cytokine secretion of human periodontal ligamental fibroblasts(PDLFs).METHODS: Before and after treatment with nicotine,the surface morphology and ultrastructure of PDLFs were observed under atomic force microscope and transmission electron microscope.The cell proliferation was examined by MTT assay.The cell cycle and apoptotic rate were determined by flow cytometry.The levels of basic fibroblast growth factor(bFGF),insulin-like growth factor I(IGF-I),transforming growth factor β1(TGF-β1),intercellular adhesion molecule 1(ICAM-1),vascular cell adhesion molecule 1(VCAM-1) and vasculr endothelial growth factor(VEGF) were detected by ELISA.RESULTS: After treatment with nicotine,pycnosis,vacuolation in the cytoplasm,and karyorrhexis were observed in the PDLFs.The rough endoplasmic reticulum expanded and mitochondria swelled.Cell proliferation was inhibited in a time-and dose-dependent manner.The cell number in G0/G1 phase increased while that in G2 phase and S phase decreased.The apoptotic rate and the rate of cycle arrest were increased with the increase in nicotine concentration.After treatment with nicotine,the secretion levels of bFGF and IGF-I declined,while the levels of ICAM-1,VCAM-1,TGF-β1 and VEGF increased.CONCLUSION: Nicotine changes the surface morphology and ultrastructure of PDLFs to apoptosis-like characters and inhibits the proliferation of the cells.Nicotine may affect the repairment of PDLFs by regulating the levels of cytokine secretion.

Aim: To research the effects of nicotine on ultrastructures and oxidative stress in human umbilical cord mesenchymal stem cells(HUCMSCs),explore mechanism of nicotine-induced apoptosis on HUCMSCs.Methods: HUCMSCs were treated with different concentrations of nicotine,ultrastructures of HUCMSCs were observed by transmission electron microscopy(TEM).The activity of catalase(CAT) was detected by visible spectrophotometer method,the activity of superoxide dismutase(SOD) was measured by xanthine oxidase assay,the activity of reduced glutathione(GSH) was detected by chemochromatometry,the content of malondialdehyde(MDA)was detected by thiobarbituric acid method.The activities of nitric oxide synthase(NOS)and inducible nitric oxide synthase(iNOS) were measured by ultraviolet spectrophotometer method.Results: After treated with nicotine,vacuole-like structures were observed in cytoplasm,the rough endoplasmic reticulum appeared to expand,and mitochondria exhibited an expanded ridge.The activities of CAT,SOD and GSH were significantly decreased,while the content of MDA was significantly increased,in a dose-dependent manner.The activities of NOS and iNOS were significantly increased in a dose-dependent manner.Conclusion: Nicotine can increase the activities of NOS,iNOS,made cellular ultrastructures of apoptosis change,generate oxidative stress,induce the imbalance of oxidants-antioxidants.

<正>烟草危害是当今世界严重的公共卫生问题之一。目前全世界每年因吸烟死亡的人数高达500多万,与烟草相关的疾病占全球死因的第一位。心血管疾病是我国首要的死亡原因,因心血管疾病死亡的患者中约30%～40%是由吸烟引起的,吸烟是心血管疾病的致病危险因素,其中,吸烟

Aim: To explore the effects of nicotine on intracellular nitric oxide,Calcium ion and expression of α7nAchR in umbilical cord mesenchymal stem cells. Methods: MSCs were treated with different concentrations of nicotine.The level of NO was detected by nitrate reductase method at 24、36、48h;after cultured with nicotine for 24h,cells were stained using by fluo-3/AM and the change of Ca2+ was determined by flow cytometer.The expression of α7nAchR was detected by Real-time Quantitative PCR. Results: After treated with nicotine,the nitric oxide level in each experimental group were significantly higher than that of the control group at 24h and 36h(P<0.05),in a dose and time dependent manners,however at 48 h the levels of NO in 0.8 mg/mL group and1.0 mg/mL group were lower than the control group,which may be related with the increased cells apoptosis.After treated with nicotine,the Ca2+ fluorescence intensity in each experimental group(0.6,0.8,1.0 mg/mL) were(141.26±16.01),(164.90±18.39),(198.76±17.63),respectively,which were higher than the control group(119.30±14.14).The expression of α7nAchR was detected in MSCs,and was found to be up-regulated after treated with nicotine in a dose-dependent manner and a time-dependent manner. Conclusion:Nicotine can promote MSCs apoptosis by up-regulating the expression of α7nAchR,stimulating MSCs to release NO and elevating the intracellular Ca2+.

<正>吸烟有害健康已成为全球关注的公共卫生问题。尼古丁是烟草中主要毒性成分之一,其吸入并沉积体内,便会导致多组织、器官的慢性损伤,引发多种疾病。成体干细胞(Adult stem cells,ASCs)是已分化组织中的一种未分化细胞,具有自我更新、免疫调节、多项分

Objective To observe the inhibition of inflammatory cytokine expressions in hearts and lungs from brain death(BD)rats pretreated with Buyang Huanwu Decoction(BYHWT).Methods Male Wistar rats,weighing from 180 to 200 g,were randomly divided into three experimental groups:control group(n=10):hearts and lungs were gotten from normal rats after anesthesia;BD group(n=10):rat brain death was gradually induced;BYHWT+BD group(n=10):7 d before BD induction,rats were ig administered with BYHWT(1.8 mL/100 g)once daily.Six hours after successful onset of BD,only the rats whose mean arterial blood pressure were more than 80 mmHg were accepted as BD donors.Hearts and lungs were then obtained.RT-PCR was used to detect the expressions of TNF-α and IL-1β mRNA.Western blotting method was applied to determining the expressions of both TNF-α and IL-1β proteins,and the phosphorylated p38 MAPK(p-p38 MAPK)proteins.Results The expressions of mRNA and protein levels of both TNF-α and IL-1β,and also the p-p38 MAPK proteins levels,were significantly enhanced in BD group compared to the control group(P0.01).While those in BYHWT+BD group were statistically decreased(P0.05)compared to BD group,but they were still significantly increased(P0.01)in comparison with the control group.Conclusion Pretreatment of the rats with BYHWT prior to the induction of rat brain death could significantly suppress the expression of inflammatory cytokines in the hearts and lungs from BD rats.This phenomenon may relate to the blockage of key target points in p38 MAPK signaling pathway.

<正>间充质干细胞(MSCs)是来源于发育早期中、外胚层的多能干细胞,存在于骨髓、胎盘、脐带血、外周血等组织中,出生后在所有组织中定居[1-2],具有向成骨细胞、成脂细胞、肝脏细胞、心肌细胞和神经细胞等多系列细胞分化潜能,且支持造血、调节免疫、对损伤的组织和器官具有良好的修复效果。MSCs体外培养扩增后保留多向分

2003年SARS全球暴发,在救治患者过程中,许多医务人员受到感染,危害甚重,医疗行业的职业危害日益受世界关注.护理人员是职业暴露较多的一个群体,由于医院管理制度不够完善,护士自身职业防护意识薄弱等诸多因素,护理职业感染风险极大,不容忽视.现将近年来国内外护士对标准预防的认知及执行情况的调查研究综述如下.

目的:研究生姜活性成分姜酚及其衍生物姜酚肟对慢性粒细胞系K562细胞的增殖活性、细胞周期及凋亡的影响.方法:采用CCK-8法检测姜酚和姜酚肟对K562细胞增殖活性的影响,PI单染检测其对K562细胞周期的影响,Annexin V-PI双染检测早期细胞凋亡,Hochest 33258染色观察细胞形态学的变化.结果:(1)姜酚作用于K562细胞48、72 h后,显著抑制K562细胞增殖,48 h的IC_(50)值为15.75 μg/mL,且具有时间及剂量依赖性.姜酚肟的抑制作用亦有时间及剂量依赖性,但较姜酚抑制作用弱.(2)姜酚15 μg/mL组细胞周期阻滞于S期,姜酚肟作用组细胞周期与对照组比较无明显差异(P＞0.05).(3)姜酚和姜酚肟作用48 h后出现早期凋亡群,姜酚各浓度组间的早期凋亡率差异显著(P＞0.05),随着药物浓度的增加凋亡率升高.(4)荧光显微间观察出现少量的细胞胞核固缩,核边集,出现凋亡小体.结论:姜酚和姜酚肟对K562细胞有显著的抑制作用,姜酚较姜酚肟抑制作用强,姜酚的抑制机制可能与影响细胞周期及诱导细胞凋亡有关,姜酚肟的抑制机制可能与诱导细胞凋亡有关.