目的:探讨合理的营养支持方式对重症急性胰腺炎(SAP)患者营养状况及预后的影响。方法:将60例SAP患者随机分为全胃肠外营养支持(对照组)和肠内与肠外相结合营养支持(实验组)两组,对比营养支持前后两组患者的血红蛋白、总蛋白、血清白蛋白、氮平衡、血脂等生化指标,每天观察相关并发症情况。结果:实验组血清白蛋白、总蛋白、血红蛋白、氮平衡方面明显优于对照组(Plt;0.05),且并发症少。结论:肠内与肠外结合的营养支持方式可以改善SAP患者的营养状况,对SAP患者治疗有积极的作用。
Schwanns cell (SC) was isolated from sciatic nerve of adult rat with Wallerine degeneration. After culture, SC-serum free culture media (SCSFCM) was obtained. By ultrafiltration with PM-10 Amicon Membrane, electrophoresis with DiscPAGE,and electrical wash-out with Biotrap apparatus, D-band protein was isolated from the SC-SFCM. The D-band protein in the concentration of 25ng/ml could affect the survival of the spinal anterior horn neuron in vitro, prominently and itsactivity was not changed after being frozen. The molecular weight of the protein ranged from 43 to 67 Kd. The D-band protein might be a neurotrophic substancedifferent from the known SCderived neurotrophic factors (NTF). Its concentration with biological activity was high enough to be detected. The advantages of MTT in assessment of NTF activity were also discussed.
Schwanns cells were obtained from the distal end of the sciatic nerve following Wallerian degeneration of SD rats. These cells were cultured with the anteriorhorn neuron of spinal cord of 14dayold SD rat fetus. The two kinds of cells were separated by a slice. Through the microscope, the dendrites and the morphology changes at the 24th, 48th, 72th, and 96 th hour after culture were observed. It was demonstrated that the Schwanns cells played the role of maintaining the survival of neuron and promoting the growth of dendrites. It was said that the Schwanns cells could secrete neurotrophic factor which made the body enlarged and caused the dendrites enlonged to several times of the body.
Objective To investigate the clinical significance of the distally-based sural musculocutaneous flap for the treatment of chronic calcaneal osteomyelitis. Methods From January 2002 to October 2005, 7 patients (4 males, 3 females; age range, 15-68 years ) were treated with the distallybased sural musculocutaneous flap, who had chronic calcanealosteomyelitis after calcaneal fracture. After the radical debridement for all the nonviable and poorly vascularized tissues, all the chronic calcaneal osteomyelitis patients, who had suffered from open calcaneal fracture or closed calcaneal fracture, were treated with the open reduction, the internal fixation, and thebone graft. The ulcer lasted for 3-12 months before diagnosis of osteomyelitis. The musculocutaneous flaps ranged in size from 8 cm×4 cm to 12 cm×7 cmand the muscle flaps ranged from 4 cm×3 cm to 6 cm×5 cm. The donor defects were closed primarily in 5 patients and were resurfaced with the splitthicknessskin graft in 2 patients. Results All the musculocutaneous flaps survived completely and all the wounds healed smoothly. All the patients followed up for 2-6 months had no recurrence of osteomyelitis or return to their preoperative ambulatory status.Conclusion It is feasible to use the distallybased sural musculocutaneous flap for treatment of chronic calcaneal osteomyelitis.
OBJECTIVE To study the protective effects of Schwann cell derived neurotrophic factor (SDNF) on motoneurons of spinal anterior horn from spinal root avulsion induced cell death. METHODS Twenty SD rats were made the animal model of C6.7 spinal root avulsion induced motoneuron degeneration, and SDNF was applied at the lesion site of spinal cord once a week. After three weeks, the C6.7 spinal region was dissected out for motoneuron count, morphological analysis and nitric oxide synthase (NOS) enzyme histochemistry. RESULTS 68.6% motoneurons of spinal anterior horn death were occurred after 3 weeks following surgery, the size of survivors was significantly atrophy and NOS positive neurons increased. However, in animals which received SDNF treatment, the death of motoneurons was significantly decreased, the atrophy of surviving motoneurons was prevented, and expression of NOS was inhibited. CONCLUSION SDNF can prevent the death of motoneurons following spinal root avulsion. Nitric oxide may play a role in these injury induced motoneuron death.
Objective To provide the anatomic basis for thedesign of the intermediate dorsal neurocutaneous flap on the foot and to reportthe clinical results. Methods On 32 adult cadaver lower limb specimens perfused with red latex, the origins, diameters, courses, branches, and distributions of the intermediate dorsal cutaneous nerve of the foot and its nutrient vessels were observed. On this anatomic basis, from June 2004 to October2005, 5 flaps were developed and applied to the repair of the soft tissue defect in the feet of 4 patients. Results The intermediate dorsal cutaneous nerve of the foot was found to arise from the superficial peroneal nerve. Crossing the intermalleolar line, it was located 1.3±0.6 cm lateral to the midpoint of the line with a diameter of 2.05±0.56 mm. The nerve stem divided into branches 2.8±1.3 cm distal to the line. They distributed the dorsal skin of the second, third and fourth metatarsal and toe. On average, 5.1 perforators per specimen were identified. At least 3 nutrient vessels were always found in each. They originated from the cutaneous branches of the anterior tibial artery and the dorsalis pedis artery in the proximal end and the dorsalis metatarsal artery in the distal end. They perforated the deep fascia 4.3±0.4 cm proximal to the intermalleolar, 1.6±0.3 cm proximal to the tip of the third toe webspace and 1.5±0.3 cm proximal to the tip of the forth toe webspace, respectively. The external diameters of them were 0.82±0.13, 0.42±0.07 and 0.49±0.09 mm, respectively. The patients were followed up for 4-10 months. All theflaps survived completely. Their appearance and function were satisfactory. Conclusion The distallybased intermediate dorsal neurocutaneousflap on the foot has an abundant blood supply. This kind of flap is especially useful in repair of the soft tissue defect in the foot.
Duchenne muscular dystrophy is an X-linked inherited progressive degenerative muscle disease caused by mutations in the dystrophin gene, and is one of the most common progressive muscular dystrophies. We will review the selection of genetic diagnosis methods for Duchenne muscular dystrophy, the selection of experimental animal models, and treatment for the primary cause (including gene replacement therapy, exon skipping therapy, genome editing, stop codon read-through therapy, and stem cell therapy), the treatment of secondary pathological reactions and methods of assessing disease progression. The purpose is to enrich clinicians’ knowledge of the disease and provide a reference and help for the clinical diagnosis and treatment of Duchenne muscular dystrophy.
Objective To investigate the origin of small saphenous vein of distally-based of sural nerve nutrient vessels flap and its clinical application. Methods The origins of nutrient vessels of small saphenousvein and communicating branches of superficial-deep vein were observed on specimens of 30 adult cadaveric low limbs by perfusing red gelatin to dissect the artery. Results The nutrient vessels of small saphenous vein originated from the heel lateral artery, the terminal perforator branches of peroneal artery and intermuscular septum perforating branches of peroneal artery. There were 2 to 5 branches ofsuch distally-based perforating branches whose diameters ranged from 0.6 to 1.0 mm. Those perforating branches included fascia branches, cutaneous branches nerve and vein nutrient branches. Those nutrient vessels formed a longitudinalvessel chain of sural nerve shaft, vessel chain of vein side and vessel networkof deep superficial fascia. The small saphenous vein had 1 to 2 communicating branches of superficial-deep vein whose diameter was 1.7±0.5 mm， 3.4±0.9 cm to the level of cusp of lateral malleolus, and converged into the fibular vein. Conclusion Distally-based sural nerve, small saphenous vein, and nutrient vessles of fascia skin have the same region. The communicating branches of superficial-deep vein is 3 to 4 cm to the level of cusp lateral malleolus. These communicating branches could improve the venousdrainage of the flap.
Objective To investigate the management of the soft tissue defect after the Achilles tendon repair. Methods From April 1996 to April 2006, 24 patients(17 males, 7 females; aged 16-59 years), who suffered from postoperative Achilles tendon exposure caused by local soft-tissue necrosis after the Achilles tendon repair, were treated and evaluated. Of the 24patients, 8 had an original open injury (machinecrush injury in 2 patients, heavy-object press injury in 3, motorcycle wheel crush injury in 3) and 16 patients had a closed injury (sports injury). In their treatment, the transferof the sural neurovascular flap was performed on 8 patients and the transfer ofthe saphenous neurovascular flap was performed on 3 patients. The secondary Achilles tendon repair was performed on 13 patients before the neurovascular flap transfer was performed. The time between the injury and the operation was 9-76 days, and the time between the Achilles tendon expousure and the operation was 3-65 days. Results All the flaps survived and the Achilles tendon exposure was well covered by the flaps of good texture. Eighteen patients followed up for 6 months to 24 months had no flap complication, and the two point discrimination of the flaps was 12-20 mm. The AOFASAnkleHindfoot Scale assessment revealed that 8 patients had an excellent result, 6 had a good result, 3 had a fair result, and just 1 had a poor result, with theexcellent and good results accounting for 77.8%. Sixteen patients (89%) were able toperform a tip-toe stance on their operative sides, and only 3 of them complained a loss of plantarflexion strength. However, 2 patients still could not perform the tip-toe stance. Conclusion The Achilles tendon repair, ifnot well performed, can result in the local soft-tissue necrosis and the subsequent Achilles tendon exposure. If those complications occur, the neurovascular flap transfer should be performed as soon as possible; if necessary, the secondary Achilles tendon repair should be performed, too.