尺神经腕背支营养血管逆行皮瓣的临床应用

目的探讨应用尺神经腕背支营养血管逆行皮瓣修复小指皮肤缺损的临床效果及手术操作要点。方法以尺神经腕背支营养血管远端为蒂,选择小指尺侧分支为皮瓣轴心血管,将皮瓣向小指远端转移,修复小指掌背侧皮肤缺损8例。结果8例全部成活,其中1例因创面止血不彻底,皮瓣受压导致远端部分坏死,经换药后痊愈。结论尺神经腕背支走向较恒定,本组未发现变异。沿皮神经干有纵行的皮神经旁血管网及皮神经干内血管网,此皮瓣血供可靠的,皮瓣切取容易,对供区影响小,是修复小指皮肤缺损的理想方法。     

Less invasive Achilles tendon reconstruction

Background  

The optimal management of chronic ruptures of the Achilles tendon is surgical reconstruction. Reconstruction of the Achilles tendon using peroneus brevis has been widely reported. Classically, these procedures involve relatively long surgical wounds in a relatively hypovascular area which is susceptible to wound breakdown.     

von Willebrand factor binding to platelet glycoprotein Ib-IX-V stimulates the assembly of an α-actinin-based signaling complex

Summary. Background: Pathological shear stress induces platelet aggregation that is dependent on von Willebrand factor (VWF) binding to glycoprotein (Gp)Ib‐IX‐V and phosphatidylinositol 3‐kinase activation. We tested the hypothesis that pathological shear stress stimulates phosphatidylinositol 3,4,5‐trisphosphate (PIP₃) synthesis by directing the assembly of a molecular signaling complex that includes class IA phosphatidylinositol 3‐kinase (PI 3‐KIA). Methods: Platelets were subjected to 120 dynes cm^?2 shear stress in a cone‐plate viscometer. Resting and sheared platelets were lyzed, immunoprecipitations of PI 3‐KIA performed, or lipids extracted for PIP₃ measurements. α‐Actinin was incubated with phosphatidylinositol 4,5‐bisphosphate (PIP₂), immunoprecipitated, and used as a substrate for in vitro PI 3‐KIA activity. Results: Pathological shear stress induces biphasic PIP₃ production. In resting platelets, PI 3‐KIA associates with α‐actinin and PIP₂. After exposure to shear stress, α‐actinin and PIP₂ rapidly disassociate from PI 3‐KIA. PI 3‐KIA then gradually re‐associates with PIP₂ and α‐actinin, and this complex becomes linked to GpIbα through the cytoskeleton. PIP₃ production and the observed changes in the association between α‐actinin, PIP₂, and PI 3‐KIA are inhibited when VWF binding to GpIbα is blocked. In a cell‐free system, α‐actinin binds PIP₂ and when the α‐actinin–PIP₂ complex is added to platelet PI 3‐KIA, PIP₃ production is stimulated. Conclusions: These results suggest that pathological shear‐induced VWF binding to GpIb‐IX‐V stimulates PIP₃ production through the assembly of an α‐actinin‐based complex that colocalizes PI 3‐KIA with substrate PIP₂.     

Arthroscopic tarsometatarsal (Lisfranc) arthrodesis

We describe an arthroscopic approach of tarsometatarsal arthrodesis for post-traumatic arthritis. Five tarsometatarsal portals (medial, P1–2, P2–3, P3–4, P4–5) are identified at the junctional points between the metatarsals by means of image intensifier. The first metatarsocuneiform joint is approached through the medial and P1–2 portal. Articular cartilage is denuded and micro-fracture of subchondral bone is performed with an arthroscopic awl. The second metatarsocuneiform joint is approached through the P1–2 and P2–3 portals and the third metatarsocuneiform joint is approached through the P2–3 and P3–4 portals. The articular surfaces are prepared for arthrodesis. The articulations are kept in desired position and transfixed with 4.0 mm cannulated screws. The fourth and fifth metatarsocuboid articulations are rarely included in the procedure. Arthroscopic arthrodesis or tendon arthroplasty of the lateral column can be performed through the P3–4 and P4–5 portals.     

Pullout reattachment of tibial avulsion fractures of the anterior cruciate ligament: a firm,effective suture-tying method using a tensioner

We describe a firm, effective suture-tying method using a tensioner for reattaching tibial avulsion fractures of the anterior cruciate ligament. Our simple method achieves strong, firm reattachment of the fracture. In addition, it prevents fixation loosening during suture tying effectively. Since pullout repair using nonabsorbable sutures is commonly used to fix various avulsion fractures, the tensioner helps attain strong, firm reattachment of avulsion fractures simply and effectively.     

Periosteal transplantation to the rabbit patella

Autologous periosteal transplantation (without chondrocyte cell transplantation) for treating traumatic articular cartilage defects of the patella gives pain relief in uncontrolled clinical studies. To study the whole transplanted area macroscopically and microscopically, animal studies are motivated. In this pilot study, we reproduce the surgical technique for periosteum transplantation on human patella to a rabbit model. A full-thickness cartilage defect of the whole patella was created in eight adult female rabbits. The defect was treated with autologous periosteal transplantation. After surgery, the rabbits were allowed free activity. This is the difference compared to the treatment in humans, where our group uses CPM for 5 days and non-weight-bearing for 12 weeks. After 21 weeks, there was a diffuse synovitis in all transplanted knees, and in five of eight knees there were signs of osteoarthritis in the patello-femoral joint. Histologically, in three animals, small islands of hyaline cartilage surrounded by fibrocartilage were seen in the transplanted area. In the other five animals, fibrocartilage was the predominant tissue. In contrast to previous experimental studies using a rabbit model, we did not achieve hyaline cartilage resurfacing.     

Nurr1基因转染人脐血间充质干细胞诱导分化为多巴胺能神经元的实验研究

目的探讨外源性Nurrl基因修饰的人脐血间充质干细胞在基因重组成纤维细胞生长因子-8(FGF8)和音猬因子(Shh)诱导下体外分化为多巴胺能神经元的情况。方法间充质干细胞被随机分为A组(对照组)、B组(Nurrl组)、C组(FGF8+Shh组)及D组(Nurrl+FGF8+Shh),采用脂质体法将pcDNA3.1-Ntrr1转染B、D组间充质干细胞,Western blot观察Nurr1基因表达情况,并在神经元条件培养液中进行增殖培养和诱导分化,间接免疫荧光染色法鉴定细胞性质,高效液相色谱法测定多巴胺含量。结果Western blot结果显示转染后Nurr1蛋白表达明显增高。A组和B组未发现酪氨酸羟化酶(TH)阳性细胞,而C组和D组TH阳性细胞分别为10．12％±2．65％及25．36％±3．13％,多巴胺含量分别为(43．6±2．1)nmol／L及(83．2±3．5)nmol／L,差异均有显著性意义(P< 0．01)。结论人脐血间充质干细胞在FGF8和Shh诱导下可以分化为多巴胺能神经元,外源性Nurr1基因修饰后,分化为多巴胺能神经元的数量增加。     

Biochemical Abnormality Associated with Smith-Lemli-Opitz Syndrome in an Infant with Features of Rutledge Multiple Congenital Anomaly Syndrome Confirms that the Latter Is a Variant of the Former

We describe a female infant with morphologic features of Rutledge multiple-congenital-anomaly syndrome (RMCAS) and biochemical features of Smith-Lemli-Opitz syndrome (SLOS). She had microcephaly with hypoplastic cerebral frontal lobes and cerebellum, agenesis of the splenium of corpus callosum, abnormal facies including hypertelorism with bilateral inner epicanthal folds, a broad nasal bridge with slightly anteverted nares and patent choanae, low set ears and complex conchal formation, high-arched palate and thick maxillary alveolar ridges, and micrognathia. Her chest was broad, genitalia were ambiguous, and uterus was bicornuate. Skeletal abnormalities included a hypoplastic appendicular skeleton, post-axial hexadactyly of the right hand and the left foot, syndactyly of bilateral 2nd-3rd toes and left 5th-6th toes, right talipes varus and left talipes valgus, and fused L5-S1 vertebrae. Congenital heart disease consisted of hypoplastic left heart, coronary sinus agenesis, ostium secundum and ostium primum defects, and a thickened septum primum. The lungs were hypolobated and the kidneys manifested oligopapillary hypoplasia. Total colonic Hirschsprung disease was noted microscopically. Analysis of liver tissue taken at postmortem examination revealed the ratio of 7-dehydrocholesterol and cholesterol to be 143 (expected, 0.28 +/- 0.28). Although initially described as a distinct syndrome, RMCAS was merged with the severe form of SLOS, because of significantly overlapping features [Online Mendelian Inheritance in Man (OMIM) #268670]. The biochemical data showing an excess of 7-dehydrocholesterol and low cholesterol in the liver tissue of our case supports this viewpoint.