Plastic repair for a case with synpolydactyly.

On March 23, 2010, we successfully treated a boy with synpolydactyly who had a total of 31 fingers and toes. Although there was bone syndactyly both the hands of the boy, one-step correction of four extremities was successful, this operation lasted 5 h and 20 min and intraoperative bleeding was about 50 ml. Skin grafting was successful after operation and all incisions healed well. The appearance and function of hands and feet were satisfactory.

Effect of 17ß-estradiol on the proliferation of condylar chondrocytes.

OBJECTIVES: To study the effects of 17ß-estradiol (E2) on the regulation of the proliferation of condylar chondrocytes and provide a preliminary discussion on the role of phosphorylate-mammalian target of rapamycin (p-mTOR) in this regulatory process. METHODS: Condylar chondrocytes were isolated from 6-week-old female rats for primary culture. Drug treatment with different concentrations of E2 and/or rapamycin (RAPA) was carried out on second-generation cells. Cell Counting Kit 8 was used to measure the cell viability of condylar chondrocytes after culture for 24, 48, or 72 h, and reverse transcription-polymerase chain reaction (RT-PCR) was applied to detect the relative gene expression of estrogen receptor alpha (ERα), estrogen receptor beta (ERß), collagen type Ⅱ (COLⅡ), autophagy-related gene 6 (Beclin-1), and autophagy-related gene 5 (ATG-5). Western blot was employed to determine the relative protein expression of ERα, ERß, Beclin-1, lipid-modified light chain 3B (LC3-Ⅱ), and p-mTOR. RESULTS: E2 could significantly promote the proliferation of chondrocytes cultured in vitro, and maximum promotion was achieved at a concentration of 10-8 mol·L-1. RAPA could significantly inhibit cell proliferation. E2 at aconcentration of 10-8 mol·L-1 could greatly improve the gene expression levels of ERα and COLⅡ (P<0.01) with the protein levels of ERα and p-mTOR (P<0.05), and decrease the gene expression levels of Beclin-1 and ATG-5 (P<0.05) with the protein levels of Beclin-1 and LC3-Ⅱ (P<0.05). RAPA could also enhance the relative protein expression of Beclin-1 and LC3-Ⅱ (P<0.01), and reduce the expression of p-mTOR (P<0.01). Treatment with the ERα antagonist significantly reduced the expression of p-mTOR in cells (P<0.01). CONCLUSIONS: At a concentration of 10-8 mol·L-1, E2 could effectively activate the phosphorylation of mTOR through the ERα-p-mTOR pathway, inhibit cell autophagy, and promote the proliferation of condylar chondrocytes.

Fasciocutaneous flap with perforating branches of peroneal artery repairing soft tissue loss in anterior and middle parts of children's feet: A STROBE-compliant article.

Repairing soft tissue loss in feet's anterior and middle parts has become a problem, especially for children. We observed the feasibility and clinical effects of superficial peroneal fasciocutaneous flap pedicled with terminal perforating branches of peroneal artery for repairing children's feet.Between January 2015 and December 2016, soft tissue loss in anterior and middle regions of feet were repaired using superficial peroneal fasciocutaneous flap pedicled with terminal perforating branches of peroneal artery in 8 children with a median age of 6.5 [4-9, interquartile range (IQR) = 3] years. The skin of lower leg was intact, and the soft tissue loss area was located in the anterior and middle regions of feet with a size of 5 cm × 4 cm to 11 cm × 7 cm combined with the exposure of tendons and joints in all the 8 children. On the basis of the conditions above, there were no indications of free skin grafting. Foot wounds were repaired all with the superficial peroneal fasciocutaneous flap pedicled with terminal perforating branches of peroneal artery (6 cm × 5 cm to 12 cm × 8 cm), and then the donor area was sutured to narrow the donor area followed by intermediate split thickness skin graft. The perforating branch trunk of peroneal artery was used as a rotation point (4 cm above the lateral malleolus) in 5 children and descending branch of perforating branch of peroneal artery as a rotation point (2 cm under the lateral malleolus) in 3 children.All flaps survived with primary healing in the 8 children. Postoperative median 7.5-month (3-12, IQR = 4.5) follow-up indicated that flap color and texture were fine, the appearances of donor and recipient areas were satisfactory, wearing shoes was not affected, and walking function and foot blood circulation were normal.For intractable soft tissue loss in the anterior and middle regions of children's feet, superficial peroneal fasciocutaneous flap pedicled with terminal perforating branches of peroneal artery can improve recipient area appearance and walking function because it has the characteristics of reliable blood supply and convenient rotation. It is worth using this method widely in clinics.

The neuroprotective mechanism of puerarin in the treatment of acute spinal ischemia-reperfusion injury is linked to cyclin-dependent kinase 5.

Puerarin is shown to exert a variety of pharmacological effects including neuroprotective properties. However, mechanisms of the action are not fully understood. This study was designed to explore the mechanism of puerarin in treatment of acute spinal ischemia-reperfusion injury in rats. Acute spinal ischemia-reperfusion injury was conducted by aortic occlusion in twenty-eight male Sprague-Dawley rats, weighting 230-250 g. The animals were randomly divided into four groups. In the animals with puerarin treatment, 50 mg/kg of puerarin was injected intraperitoneally after reperfusion, and followed by the same dose of injection every 24h for 2 days. In the animals with roscovitine pre-treatment, 30 mg/kg roscovitine was intravenously administrated 60 min before spinal ischemia started. After spinal ischemia for 60 min followed by 48 h of reperfusion, the motor function, spinal infarction volume, apoptosis indices and the activities of Cdk5 and p25 were examined. Acute spinal ischemia-reperfusion resulted in an injury of the spines associated with motor deficit, elevation of Cdk5 and p25 activities, and increase in the spinal apoptosis number and spinal infarction volume. Puerarin improved motor function associated with the decreased apoptosis number, spinal infarction volume, and Cdk5 and p25 activities. The present study indicated that reduction of spinal injury was associated with inhibition of Cdk5 and p25, and that inhibition of Cdk5 and p25 was one of the neuroprotective mechanisms in the puerarin treatment of acute ischemia/reperfusion-induced spinal injury in rats.

Venous arterialization for the treatment of large-area foot skin retrograde avulsion.

Between 2009 and 2011, three patients with large-area foot skin retrograde avulsion (more than 1% of the body surface area) underwent venous arterialization. Anastomosis of the artery in the wound surface with the vein in the skin flap and an appropriate number of venous end-to-end anastomoses were performed. The skin flaps survived in all 3 patients. Six months postoperatively, the flap elasticity and appearance were close to that of normal skin, and foot function was better without scar contracture. When venous arterialization is used to treat foot avulsion, the following points should be noted. Surgical indications include no fresh bleeding from the wound edge of the avulsed skin after debridement, more complete avulsed skin, and superficial veins that do not completely separate from the avulsed skin. Venous arterialization is not suitable to avulsion with fresh bleeding, avulsed skin in small fragments, and avulsion with a subcutaneous venous network embolism. During debridement, the subcutaneous venous network should be protected to avoid exposing the vein stems outside the fat layer. If the avulsion is less than 1% of the body surface area, arterial-venous anastomosis can provide adequate blood supply. Venous-venous anastomosis is performed as much as possible to enhance venous return and decrease microcirculatory pressure, which is conducive to the establishment of effective blood circulation.

The neuroprotective mechanism of puerarin treatment of acute spinal cord injury in rats.

Puerarin extracted from radix puraeriae is shown to exert a variety of pharmacological effects including neuroprotective properties. However, its mechanisms of action are needed to further explore. The study was designed to investigate the mechanism of puerarin treatment of acute spinal cord ischemia-reperfusion injury (SCI/RI) in rats. SCI/RI was conducted in male Sprague-Dawley rats, and 50mg/kg of puerarin was injected intraperitoneally at 1, 2, 4 and 6h after reperfusion, followed by the same dose of injection every 24h for 2 days. Glutamate level, metabotropic glutamate receptors (mGluR) mRNA expression, and apoptosis indices were examined. Neurologic function was assessed at 48 h of reperfusion. SCI/RI caused extensive motor deficit associated with an elevation of glutamate level and mGluRs-1 mRNA expression, while puerarin administration improved motor deficit, and decreased glutamate level and inhibited mGluRs-1 mRNA expression. The present study demonstrated that administration of puerarin reduced the spinal ischemia/reperfusion injury, and suggested that the neuroprotective mechanism of puerarin involved a decrease in glutamate release and mGluRs-1 mRNA expression.

Treatment of severe hand deformities caused by epidermolysis bullosa.

Little research has been done regarding the treatment of severe hand deformities caused by epidermolysis bullosa. A 14-year-old boy was diagnosed with congenital epidermolysis bullosa. He was treated in our hospital several times, but the pathogenetic condition worsened. On examination, both hands were clenched fists and had scar formation. Skin fusion was observed between the 5 fingers. Nails were absent and the thumb was in the fist. His fingers were short, and active and passive flexion and extension could not be performed. The right hand was treated first. After the adhesions were separated, we found that the 5 fingers were connected by dermis. After the dermis was separated and the hand was fixed in the extension position, there were small cutaneous deficiencies. The fingers were fixed in the functional position with Kirschner wires. The wound surface was covered with self-made aureomycin ointment gauze. After regular dressing changes for 6 weeks, the wound surface was completely healed. After 3 months of rehabilitation training, most hand function was recovered.Based on our findings in this case, when treating patients with epidermolysis bullosa, physicians must carefully observe whether enough dermis exists to avoid an unnecessary skin graft. We also found that the quality of skin used in skingrafting is questionable due to pathological changes in the skin. If there is enough dermis and the cutaneous deficiency is smaller after contracture release, the covering of drug dressings on the cutaneous deficiency is more conducive to the recovery of limb function and the reduction of damage to the donor sites.

The optimal therapeutic timing and mechanism of puerarin treatment of spinal cord ischemia-reperfusion injury in rats.

AIM OF THE STUDY: The purpose of this study was to explore the optimal therapeutic timing and mechanism of puerarin treatment of spinal cord ischemia-reperfusion injury. MATERIALS AND METHODS: The spinal ischemia-reperfusion injury was conducted in male Sprague-Dawley rats, and 50mg/kg of puerarin was injected intraperitoneally at 1, 2, 4 and 6h after the injury. Motor function was measured 48 h after reperfusion started. Thioredoxin expression and apoptosis indices were determined. RESULTS: Improvement of motor function at 1, 2, and 4h was demonstrated in the animals with puerarin treatment. Ischemia-reperfusion injury resulted in a decrease in the expression of thioredoxin, while puerarin administration elevated the expression of thioredoxin-1/thioredoxin-2 mRNA. Apoptosis indices were significantly reduced by puerarin administration. CONCLUSIONS: We conclude that administration of puerarin within 4h of spinal ischemia-reperfusion injury reduces ischemic reperfusion damage, and that the neuroprotective effect of puerarin involves an increase in the transcription of thioredoxin and a reduction of apoptosis.