骨外露及皮肤软组织缺损的修复

目的　评价和探讨修复骨外露及皮肤软组织缺损的各种方法 ,使其更好地用于临床。方法　 3 5例不同部位的骨外露分别采用皮片移植、皮瓣及肌皮瓣转移、皮瓣及肌皮瓣游离移植等方法 ,覆盖外露的骨面。结果　 3 1例全部存活 ,1例皮瓣部分坏死 ,2例创口延迟愈合 ,1例游离皮瓣失败。结论　对骨外露及皮肤软组织缺损应尽量在早期修复 ,最常用的方法是皮瓣及肌皮瓣的转移或移植。     

窒息鼠脑组织型纤溶酶原激活物活性变化与脑水肿的关系

目的：探讨窒息对鼠脑分泌组织型纤溶酶原激活物（TPA）的影响与脑水肿的关系。方法：通过“延迟剖宫产术”致胎鼠宫内窘迫，实验分空白对照组，窒息15min组，窒息30min组，窒息15min复氧30min组，窒息30min复氧30min五个实验组，每组各取8例测试脑组织TAP的活性及含水量，结果：窒息后鼠脑TPA活性与含水量均升高（P＜0．01），结论：窒息可致TAP活性增高，同时发生脑水肿，高活性的TPA可能是脑缺氧缺血致不可逆神经元损伤的一个重要媒介。     

抑制脑血栓形成的硫代磷酸酯脱氧寡核苷酸的亲和性研究

目的为抑制脑血栓形成,合成与TF基因启动子区切应力反应元件(SSRE)形成三链DNA的硫代磷酸酯寡核苷酸(TFO)。方法设计TFO序列14条,采用固相亚磷酰胺三酯固相法合成TFO。硫代磷酸酯修饰在TFO的3'末端进行。应用电泳迁移分析(EMSA)观察寡核苷酸和硫代脱氧寡核苷酸的亲和性。结果在设计合成的14条寡核苷酸中,与靶序列能形成三链DNA的TFO只有T21GTa、T14GTa和T15GTa,其Kd值分别为3.6×10-10、1.0×10-9和1.0×10-8(M),经硫代磷酸酯修饰后分别为:2.3×10-9、3.8×10-9和1.5×10-8。结论硫代磷酸酯修饰的T21GTa-ps、T14GTa-ps和T15GTa-ps能够与TF基因启动子SSRE的3个位点形成三链DNA。     

The surgical management of resistant club foot by rotation skin flap and extensive soft tissue release

Summary Resistant club foot remains an unsolved problem because of the complex aetiological and pathological factors, and is still seen quite frequently, especially in developing countries. The posteromedial skin contracture is a potent deforming force which is responsible for many failures or relapses. I report the results of an operation in which a rotation skin flap was combined with an extensive soft-tissue release. The age of the children was from 9 months to 10 years. The follow-up period was from one to 9 years with an average of 43 months, and in 50 cases for more than 5 years. I consider that the outcome has been excellent or good in 94 out of 100 feet.

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Résumé Le pied bot invétéré demeure un problème mal résolu en raison de la complexité des facteurs étiologiques et anatomiques et il est encore bien souvent rencontré, notamment dans les pays en voie de développement. La rétraction cutanée postéro-interne représente un puissant élément de la déformation, qui est responsable de bon nombre d'échecs ou de récidives. Nous rapportons les résultats d'une opération qui associe un lambeau cutané de rotation à la libération des parties molles. L'âge des enfants était compris entre neuf mois et dix ans. Le recul est de un à neuf ans, avec une moyenne de 43 mois. Cinquante enfants ont été suivis plus de cinq ans. Les résultats sont excellents ou bons dans 94% des cas.

     

Study on the Mechanism of the Annexin I -Mediated Co-Assembly of t-PA and Plasminogen

In order to further investigate the effect of annexin Ⅱ (Ann- Ⅱ ) on tissue plasminogen activator (t-PA)-dependent plasminogen (PLG) activation and its interactive mechanism, recombinant native Ann- Ⅱ bound t-PA, PLG and plasmin with high affinity was examined. The flow cytometric assay showed that the ann- Ⅱ expression rate was higher in the human umbilical vein endothelial cell (HUVEC) (87. 65 %) than in the HL-60 cells as controls (35. 79 %). Two irrelevant proteins,bovine serum albumin (BSA) and equine IgG (EIG) had no effect on the production of plasmin.Ann- Ⅱ -mediated enhancement of t-PA-dependent PLG activation was inhibited by ε-aminocaproic acid or by pretreatment of Ann- Ⅱ with carboxypeptidase B with the inhibitive rate being 77.8 % and 77. 0 %, respectively. It was revealed that the effect of Ann- Ⅱ on PLG activation was specific for tPA. Urokinase didn‘t bind to Ann- Ⅱ , demonstrating the role of receptor-related lysine residues on activation of PLG, showing that the Ann- Ⅱ -PLG interaction was dependent upon carboxyl-terminal lysine residues. These findings suggest that annexin Ⅱ -mediated co-assembly of t-PA and PLG may promote plasmin generation and play a key role in modulating fibrinolysis on the endothelial surface.     

Adipose tissue as target organ in the treatment of hormone-dependent breast cancer: new therapeutic perspectives

Breast cancer is the female malignant neoplasia with the highest incidence in the industrialized world. Despite many undeniable therapeutic successes obtained, breast cancer still remains, however, a major health issue. In the last few years, thanks to aromatase inhibitors, the hormone therapy for oestrogen-dependent breast cancer has evolved in terms of efficacy and tolerability; at the same time, it has enabled us to better define the role of oestrogens in the etiopathogenesis of this tumour. Weight increase and obesity have been identified as the most important risk and prognostic factors for breast cancer in postmenopausal women. Several hypotheses have been proposed to explain the association of obesity with postmenopausal breast cancer. A more recent hypothesis suggests that adipocytes and their autocrine (paracrine and endocrine actions) are at the centre of such an etiopathogenetic mechanism. A better understanding of the main mechanisms that link together menopause, body-weight increase and hormone-dependent breast cancer is paramount to enable the identification of key molecules involved in the development of breast carcinoma and suggest new therapeutic options. The present review will discuss important findings on the therapeutic aspects of adipose tissue and adipokines as a target for treatment of hormone-dependent breast cancer.     

Necrotizing soft tissue infections

Necrotizing soft tissue infections (NSTI) represent a spectrum of diseases characterized by extensive rapidly progressive necrosis that may involve the skin, subcutaneous tissues, fascia or muscle. Their progress is extremely fast, leading often to sepsis and septic shock that ends up in multiple organ failure with abrupt and high mortality. A variety of classification systems have been developed based on parameters such as anatomic location of the disease or microbiology. There are a number of factors that predispose to the spread of these soft tissue infections, such as delays in recognition, immune suppression, diabetes mellitus and advanced age. The use of broad‐spectrum antibiotics tends to mask the severity of the underlying infection, modulates the clinical presentation, and even delays hospital admission. The most important factor affecting outcome in NSTI is early diagnosis and aggressive radical surgical treatment. The medical records of 13 patients who had been treated for NSTI from 1996 to 2005 were reviewed, retrospectively. There were eight men (61.5%) and five (38.5%) women. Mean age was 56 years (range 27–73). Seven cases of infection involved the perineal region (54%), two the lower limb, one the upper limb and three the abdominal wall/trunk. The most common associated comorbidity was diabetes mellitus in five patients (38.5%). A single organism was identified in two (15%) and multiple organisms in 11 (85%) patients. Necrotizing aponeurositis Type I was the most common of the polymicrobial necrotizing infections. Overall survival was 85%, and the mean hospital stay for survivors was 35 days (range 17–92).     

Sutureless bowel anastomosis using Nd:YAG laser

Small bowel anastomoses were performed without sutures by using the Nd:YAG laser to produce welded enterotomies. Optimal energy levels for contact and noncontact laser were determined. Anastomoses produced using five target energy levels between 100 and 500 J were examined. Short-term anastomotic strength of these enterotomies was measured 1 min after the welding. Bursting pressure of the laser welded enterotomies was compared to the bursting pressure of traditional two-layer, inverting, interrupted sutured bowel anastomoses. The overall mean bursting pressure of non-contact-welded enterotomies was 50.6 mmHg. Optimal laser settings determined in this initial phase were then used to produce anastomoses in rabbits which are recovered postoperatively for 1 or 2 weeks in order to examine long-term viability and integrity of the anastomoses. All chronic rabbit preparations recovered without complication. The mean bursting pressure was 200 mmHg, not significantly different from that of uncut bowel or two-layer sutured anastomosis.     

神经内结缔组织增生与三叉神经脱髓鞘的关系

目的探讨三叉神经痛（trigeminal neuralgia，TN）患者三叉神经患支内结缔组织改变与神经脱髓鞘的关系。方法对手术切取的TN患者三又神经患支标本及对照标本行髓鞘染色，在光镜及电镜下观察神经横截面形态改变，并采用图像分析仪进行半定量测量。结果形态观察及图像分析结果都显示TN患者三叉神经患支明显脱髓鞘，神经内结缔组织显著增生，F检验证实二者存在显著线性正相关。结论TN患者三叉神经惠支内神经内结缔组织增生，可能是TN发生的重要机制之一。