Syncytin与滋养细胞融合

Syncytin是人类内源性逆转录病毒HERV—W基因编码的膜糖蛋白，主要在胎盘合体滋养细胞表达。Syncytin可促进滋养细胞的融合，它的表达异常与妊娠高血压综合征、21-三体综合征等病理妊娠有关。     

PCNA、Survivin蛋白在人绒癌细胞株BeWo合体化过程中表达变化的研究

目的:通过检测人绒癌细胞株Be Wo合体化过程中增殖细胞核抗原(proliferating cell nuclear antigen,PCNA)、生存素(Survivin)蛋白表达的变化,探讨滋养细胞合体化后增殖性的变化,为恶性滋养细胞肿瘤,尤其是耐药恶性滋养细胞肿瘤的临床治疗提供新的思路和方法。方法:利用毛喉素(forskolin)诱导Be Wo细胞株融合;应用逆转录聚合酶链反应(RT-PCR)检测促融素(Syncytin)在forskolin作用不同时间的Be Wo细胞株中的表达;应用蛋白质印迹(Western blotting)检测PCNA、Survivin蛋白在forskolin作用不同时间的Be Wo细胞株中的表达;应用噻唑蓝比色分析实验(MTT)法检测forskolin作用不同时间的绒癌细胞株Be Wo的增殖能力。结果:1forskolin作用后的Be Wo细胞株Syncytin基因的表达增强,且随着forskolin作用时间的延长,Syncytin的表达更强,于48 h达到高峰。2forskolin作用后的Be Wo细胞株PCNA、Survivin蛋白的表达降低。3forskolin作用后的Be Wo细胞株的增殖能力下降,且不同作用时间的差异有统计学意义;forskolin作用的时间越长,Be Wo细胞株增殖能力下降越明显。结论:人绒癌细胞株Be Wo合体化后PCNA、Survivin蛋白的表达降低,说明人绒癌细胞株Be Wo合体化后增殖性降低,推测诱导滋养细胞合体化可能对临床治疗恶性滋养细胞肿瘤具有一定作用。     

正常妊娠及病理妊娠胎盘滋养细胞CD3的表达及其与FasL的表达的关系

[目的]研究胎盘滋养细胞CD3与FasL表达的相关性及其临床意义.[方法]采用免疫组织化学SP法检测52例正常妊娠及96例病理妊娠胎盘组织中CD3及FasL的表达.[结果]正常妊娠胎盘滋养细胞在表达FasL的同时,有CD3表达于细胞膜上,在妊娠高血压综合征(妊高征)、胎儿窘迫、早产3组患者胎盘滋养细胞中其强度与FasL的表达呈正相关.[结论]妊高征、胎儿窘迫、早产的胎盘绒毛发育不全、功能下降等一系列的免疫病理改变可能与胎盘滋养细胞表面CD3及FasL表达减少有关.     

病理妊娠胎盘滋养细胞FasL的表达

目的:比较正常妊娠与病理妊娠胎盘滋养细胞Fas L的表达,从免疫学角度分析病理妊娠的可能发病机制。方法:采用免疫组织化学SP法检测96例病理妊娠患者胎盘组织中FasL的表达,通过高清晰彩色病理免疫组化测量系统对其定量分析,取52例正常孕妇胎盘作对照进行比较。结果:病理妊娠组中妊娠高血压综合征(妊高征)、胎儿窘迫、早产3组患者胎盘滋养细胞表面FasL表达面积明显低于正常组(P<0.01),且3组胎盘滋养细胞表面FasL表达强度(包括平均光度及积分光度)也明显低于正常组(P<0.01),但3组间差异无显著意义(P>0.05)。结论:妊高征、胎儿窘迫、早产的胎盘绒毛发育不全、功能下降等一系列的免疫病理改变可能与胎盘滋养细胞表面FasL表达减少有关。     

低氧诱导因子-1与妊高征发病的研究进展

滋养细胞浅着床是妊娠期高血压疾病发病的关键环节 ,而滋养细胞的浸润深度直接影响到妊高征的发病。近年来关于低氧诱导因子 1在早孕滋养细胞浸润中的作用及在妊娠高血压综合征胎盘中的表达情况时有报道。该文对此加以综合分析 ,认为低氧诱导因子 1通过影响滋养细胞分化及浸润 ,可能在妊高征发病中起到关键作用     

hCG、hPL与妊娠高血压综合征

人绒毛膜促性腺激素、人胎盘生乳素是胎盘滋养细胞合成和分泌的肽类激素。妊娠高血压综合征可能是滋养细胞的功能紊乱结果 ,人绒毛膜促性腺激素及人胎盘生乳素水平异常与妊娠高血压综合征有关 ,其水平的变化可能对妊娠高血压综合征有预测和监测作用。     

p57kip2和cyclinE在妊娠滋养细胞肿瘤中的表达和意义

目的 探讨p57kip2和cyclin E在妊娠滋养细胞肿瘤中的表达及意义.方法 应用免疫组织化学法检测32例妊娠滋养细胞肿瘤组织中p57kip2和cyclin E的表达情况,以正常早孕绒毛14例、葡萄胎首次清宫组织34例为对照.结果 在正常早孕绒毛、葡萄胎、妊娠滋养细胞肿瘤组织的滋养细胞中,p57kip2的阳性表达率分别是57.14%、50.00%、3.13%,随着滋养细胞疾病恶性程度的增加,p57kip2染色阳性细胞数及染色强度降低,经比较有显著性差异(χ2=14.788,P<0.001);cyclin E的阳性表达率分别是78.57%、44.12%、46.88%,cyclin E在葡萄胎、妊娠滋养细胞肿瘤组染色阳性细胞数及染色强度较正常早孕绒毛降低,经比较有显著性差异(χ2=3.982,P=0.046),但在葡萄胎、妊娠滋养细胞肿瘤组中无显著性差异(P=0.822).在妊娠滋养细胞肿瘤组织中,p57kip2和cyclin E的表达与临床病理特征之间无关(均P>0.05).结论 p57kip2的低表达可能是妊娠滋养细胞肿瘤形成过程中的早期事件,并参与了妊娠滋养细胞肿瘤的发展;cyclin E的异常表达与妊娠滋养细胞肿瘤无关.     

hCG、hPL与妊娠高血压综合征

人绒毛膜促性腺激素、人胎盘生乳素是胎盘滋养细胞合成和分泌的肽类激素。妊娠高血压综合征可能是滋养细胞的功能紊乱结果，人绒毛膜促性腺激素及人胎盘生乳素水平异常与妊娠高血压综合征有关，其水平的变化可能对妊娠高血压综合征有预测和监测作用。     

低氧诱导因子-1与妊高征发病的研究进展

滋养细胞浅着床是妊娠期高血压疾病发病的关键环节，而滋养细胞的浸润深度直接影响到妊高征的发病。近年来关于低氧诱导因子-1在早孕滋养细胞浸润中的作用及在妊娠高血压综合征胎盘中的表达情况时有报道。该文对此加以综合分析，认为低氧诱导因子-1通过影响滋养细胞分化及浸润，可能在妊高征发病中起到关键作用。     

Fas/Fasl系统与妊高征的关系

死亡因子Fas与其配体Fasl相结合可诱导细胞凋亡 ,这一过程作为组织更新手段伴随着胎盘的发育 ,正常妊娠Fas/Fasl表达与胎盘生长、滋养细胞侵入均有关系 ,并在一定程度上达到平衡。妊娠高血压综合征时胎盘细胞凋亡增加 ,Fas/Fasl表达异常可部分解释胎盘浅着床和局部免疫反应增强 ,但其敏感性与表达不一致应进一步研究     

Toxic shock syndrome: broadening the differential diagnosis

BACKGROUND: Toxic shock syndrome is a rare but potentially fatal toxin-mediated febrile illness. Although classically associated with tampon use, it is now known that many nonmenstrual conditions are related to this syndrome. Serious morbidity and mortality can occur if this syndrome is not promptly recognized. METHODS: MEDLINE was searched from 1978 to the present using the phrase "toxic shock syndrome." Case reports and articles related to tampon-associated toxic shock syndrome were excluded from the literature review except when defining toxic shock syndrome or discussing the cause of the syndrome. A case of nonmenstrual toxic shock syndrome associated with an intrauterine device and a review of the definition, cause, diagnostic criteria, and management are reported. RESULTS AND CONCLUSIONS: Toxic shock syndrome can mimic many common diseases. Because it can be associated with a number of nonmenstrual-related conditions, patients with unexplained fever and rash and a toxic condition out of proportion to local findings should have the diagnosis of toxic shock syndrome in their differential diagnosis. Early recognition and aggressive management can decrease the overall morbidity and mortality.     

Genetics of the metabolic syndrome

The clustering of cardiovascular risk factors such as abdominal obesity, hypertension, dyslipidaemia and glucose intolerance in the same persons has been called the metabolic or insulin-resistance syndrome. In 1998 WHO proposed a unifying definition for the syndrome and chose to call it the metabolic syndrome rather than the insulin-resistance syndrome. Although insulin resistance has been considered as a common denominator for the different components of the syndrome, there is still debate as to whether it is pathogenically involved in all of the different components of the syndrome. Clustering of the syndrome in families suggests a genetic component. It is plausible that so-called thrifty genes, which have ensured optimal storage of energy during periods of fasting, could contribute to the phenotype of the metabolic syndrome. Common variants in a number of candidate genes influencing fat and glucose metabolism can probably, together with environmental triggers, increase susceptibility to the syndrome. Among these, the genes for beta 3-adrenergic receptor, hormone-sensitive lipase, lipoprotein lipase, IRS-1, PC-1, skeletal muscle glycogen synthase, etc. appear to increase the risk of the metabolic syndrome. In addition, novel genes may be identified by genome-wide searches.     

Nephrotic syndrome in Hodgkin's disease

The authors are presenting a rare paraneoplastic syndrome in Hodgkin's disease. Young female patient presented with symptoms of nephrotic syndrome. Renal biopsy showed mesangiocapillary glomerulonephritis. Remission was achieved with combined therapy. Four months later, when the nephrosis syndrome relapsed, Hodgkin's disease was diagnosed (nodular sclerosing subtype). Hodgkin's disease was staged as III/BS. Polychemotherapy resulted complete remission of both Hodgkin's disease and nephrotic syndrome. Causes of nephrotic syndrome in Hodgkin's disease can include renal vein thrombosis, amyloidosis or paraneoplastic syndrome. Nephrotic syndrome in Hodgkin's disease may relate to dysfunction of T-cells or altered cytokine balance, but the exact pathogenesis is not known. This case attracts attention that a rare cause of nephrotic syndrome can be Hodgkin's disease.     

Periodically leaking capillaries

The systemic capillary leak syndrome (Clarkson's syndrome) is a rare idiopathic disorder, characterized by recurrent episodes of hypovolaemic shock, haemoconcentration and hypoalbuminaemia due to a sudden shift of fluid and macromolecules from the intravascular to the interstitial space. A young man is presented in whom recurrent attacks of hypotension and diffuse swelling were initially attributed to staphylococcal toxic shock syndrome. With the additional finding of a monoclonal gammopathy, the diagnosis of systemic capillary leak syndrome was made. Recognition of this syndrome is important, as prophylactic treatment with terbutaline and theophylline may be beneficial in this life threatening syndrome.     

Refeeding syndrome with enteral nutrition in children: a case report,literature review and clinical guidelines

Refeeding syndrome is a potentially fatal complication of the nutritional management of severely malnourished patients. The syndrome almost always develops during the early stages of refeeding. It can be associated with a severe derangement in electrolyte and fluid balance, and result in significant morbidity and mortality. It is most often reported in adults receiving total parenteral nutrition (TPN), although refeeding with enteral feeds can also precipitate this syndrome.We report what we believe to be the first case of refeeding syndrome in an adolescent with newly diagnosed Crohn's disease. This developed within a few days of starting exclusive polymeric enteral nutrition. A systematic literature review revealed 27 children who developed refeeding syndrome after oral/enteral feeding. Of these, nine died as a direct result of complications of this syndrome. We discuss the implications of this syndrome on clinical practice and propose evidence-based guidelines for its management.     

XYY综合征患儿的认知

XYY综合征又被称为超雄综合征,是位居克氏综合征之后常见的男性性染色体疾病。XYY综合征的临床表型差异大。既往XYY综合征检出率较低,但是随着产前诊断技术的发展及妊娠夫妇对胎儿重视程度的增加,产前诊断为胎儿合并XYY综合征的病例增多。目前,宫内诊断胎儿合并XYY综合征后,需要多学科团队专家评估胎儿预后,对妊娠夫妇提供详细、无偏倚的临床咨询。XYY综合征患儿出生后,仍然需要多学科团队专家协作,对部分XYY综合征患儿发生的行为认知问题,进行康复训练及临床干预。对发现XYY综合征患者的育龄期夫妇,需要采取辅助生殖技术,提高其妊娠率及避免不良妊娠结局发生。笔者拟从XYY综合征患儿的遗传学背景、诊断、胎儿围生结局及出生后生存情况、临床表型、胎儿情况评估及处理等方面的最新研究进展进行阐述,旨在为可能孕育XYY综合征患儿的育龄期夫妇提供临床咨询参考。     

Weight Loss and Medication in Polycystic Ovary Syndrome Therapy

Polycystic ovary syndrome, which is a complex syndrome, affects approximately 6% of reproductive-age women. Many abnormalities are associated with polycystic ovary syndrome, but confusion still exists about their causation. Diagnosis of polycystic ovary syndrome is by exclusion. Management of the metabolic aspects of polycystic ovary syndrome focuses on minimizing insulin resistance and hyperinsulinemia with diet therapy or insulin-lowering drugs.     

Hypokalemic nephropathy in an adult patient with partial empty sella: a classic Bartter's syndrome, a Gitelman's syndrome or both?

Bartter's syndrome belongs to a group of hypokalemic renal channel diseases. These channels are located in the lipid layer of cell membranes where they exist as water channels through which ion transport is performed. Based on the type of genetic disorder and clinical presentation, Bartter's syndrome is classified as neonatal, classical and Gitelman's syndrome. Most of the cases have been noted in pediatric age groups and adult-onset cases are very rare. Moreover, an association between Bartter's syndrome and empty sella has recently been reported in 3 children. We report here the second case of an adult patient affected by Bartter's syndrome with partial empty sella. The patient showed some clinical and histological characteristics of both classic Bartter's syndrome and Gitelman's syndrome, suggesting that genotype and phenotype of Bartter's syndrome are not so clear-cut and that phenotypic overlap may occur, according to a recent hypothesis. Magnetic resonance imaging disclosed a partial empty sella. A thorough endocrinological investigation showed normal hypophyseal, thyroidal, adrenal and gonadal function. Good therapeutic effects were achieved using spironolactone, ACE-inhibitor and potassium supplementation, with normalization of the kalemia. At present, the value of the association of Bartter's syndrome and empty sella remains unclear and future studies are needed to clarify the importance of this association, both in children and in adult patients affected by Bartter's syndrome.     

运动疗法在慢性疲劳综合征治疗中的作用探讨

为探讨运动疗法治疗慢性疲劳综合征的疗效,本文主要从慢性疲劳综合征的概念,流行特征及诊断标准的阐述基础上,分析了运动疗法在治疗慢性疲劳综合征中的研究进展,并对运动疗法的连一步应用做了展望.结果发现运动疗法治疗慢性疲劳综合征缺乏系统有效的方法及临床试验,对于是否能够治愈慢性疲劳综合征还存在争议,需要大量的实验依据进行证明,但运动疗法对改善患者的症状,提高其免疫能力已取得基本一致的结论,适量有规律的运动治疗慢性疲劳综合征能取得较为理想的效果,值得广大学者深入研究和推广应用.     

Kearns-Sayre syndrome associated with de Toni-Debré-Fanconi syndrome due to cytochrome-c-oxidase (COX) deficiency

We report a 43-year-old female with complete Kearns-Sayre syndrome, focal deficiency of cytochrome-c-oxidase (COX) and extensive deletion of the mtDNA in muscle fibers, which showed progressive insufficiency of the renal tubule: first hyperphosphaturia and hyperaminoaciduria and, later, also glucosuria (de Toni-Debré-Fanconi syndrome), a syndrome to date rarely diagnosed in association with complete Kearns-Sayre syndrome. In our opinion, this case, in view of the relationships between retinal and kidney disorders, suggests a search for de Toni-Debré-Fanconi syndrome in all patients with Kearns-Sayre syndrome also by quantitative and chromatographic methods for the assessment of aminoacids, phosphates and sugars in the urine.