[Revision of Schatzker type â ¥ tibial plateau fracture failure focus on the recovery of lower limb alignment].

Objective: To explore the influence of the lower extremity abnormal alignment and the joint surface, and to explore the surgical skills. Methods: Twenty-two cases of tibial plateau Schatzker Ⅵ fracture internal fixation failure revision from January 2012 to January 2017 in Department of Orthopedics, Shanghai 10(th) Hospital.One year follow-up after initial surgery to make sure of failure.Three-dimensional CT scan, radiography, infection index, gait analysis, knee joint ROM, femur tibia angle, tibial plateau tibial shaft angle and posterior slope if tibial plateau were observed. The medial approach and bi-planer osteotoma were used.Autogenous iliac bone graft, postoperative fast recovery channel were used.Follow-up point included preoperative and postoperative 7 days, 6 weeks, 3 months, and 6 months.Obvervational index included double lower limbs radiography, knee society score(KSS), complications such as infection, skin necrosis, joint main passive activity, double lower limbs alignment the last follow-up SF-36 scale.Rate was compared by χ(2) test, measurement data using paired sample t test.Correlation was analyzed by Pearson correlation regression testing. Results: Twenty-two patients received follow-up.KSS, more than 21 cases were benign, with good gait.One case was poor, with claudication gait.Not skin necrosis, no deep infection cases, 1 case get blisters 2 days postoperatively, and disappear after 5 days with detumescence and cold therapy.Whether restoring force line affect the KSS significantly(χ(2)=22.000, P=0.000). Knee joint ROM, SF-36 score, KSS and lower limb alignment were improved significantly. In different individual the articular surface and anatomical angle recovered greatly but the posterior slope angle was quite difference which has no correlation with KSS and SF-36 scale(P>0.01). Conclusions: Revision of Schatzker type Ⅵ tibial plateau fracture failure should focus on the recovery of lower limb alignment.moderate overcorrect bone cutting and joint surface height can bring benefits to the postoperative knee function.Revision surgery patients have greater psychological pressure, more early psychological intervention is necessary.

A new species of Triplophysa (Nemacheilidae: Cypriniformes), from Guangxi, southern China.

A new species, Triplophysa huapingensis, is described from the Hongshuihe River, Guangxi, China. The new species is distinguished from other species of Triplophysa by the following combination of characters: body covered with scales, lateral line complete, eyes not degenerate, dorsal fin truncate, caudal fin forked, tip of pelvic fin not reaching anus, eight branched rays of dorsal fin, six branched rays of pelvic fin, 16 branched rays of caudal fin, grey and black diffused blotches on dorsal and lateral head and body. A key to all recorded species of Triplophysa in the Xijiang River system is provided.

Therapeutic angiogenesis. A single intraarterial bolus of vascular endothelial growth factor augments revascularization in a rabbit ischemic hind limb model.

Vascular endothelial growth factor (VEGF) is a heparin-binding, endothelial cell-specific mitogen. Previous studies have suggested that VEGF is a regulator of naturally occurring physiologic and pathologic angiogenesis. In this study we investigated the hypothesis that the angiogenic potential of VEGF is sufficient to constitute a therapeutic effect. The soluble 165-amino acid isoform of VEGF was administered as a single intra-arterial bolus to the internal iliac artery of rabbits in which the ipsilateral femoral artery was excised to induce severe, unilateral hind limb ischemia. Doses of 500-1,000 micrograms of VEGF produced statistically significant augmentation of collateral vessel development by angiography as well as the number of capillaries by histology; consequent amelioration of the hemodynamic deficit in the ischemic limb was significantly greater in animals receiving VEGF than in nontreated controls (calf blood pressure ratio, 0.75 +/- 0.14 vs. 0.48 +/- 0.19, P < 0.05). Serial angiograms disclosed progressive linear extension of the collateral artery of origin (stem artery) to the distal point of parent vessel (reentry artery) reconstitution in seven of nine VEGF-treated animals. These findings establish proof of principle for the concept that the angiogenic activity of VEGF is sufficiently potent to achieve therapeutic benefit. Such a strategy might ultimately be applicable to patients with severe limb ischemia secondary to arterial occlusive disease.

Low-efficiency of percutaneous adenovirus-mediated arterial gene transfer in the atherosclerotic rabbit.

Recombinant adenoviruses are the most efficient vectors with which to perform arterial gene transfer. Previous in vivo studies of adenovirus-mediated arterial transfection, however, have been performed using normal or endothelium-denuded arteries. It is unclear whether these results can be extended to atherosclerotic arteries. Accordingly, this study was designed to (a) assess the feasibility of adenovirus-mediated gene transfer to atherosclerotic lesions, and (b) compare the transfection efficiency, anatomic distribution of transfected cells, and duration of transgene expression achieved in normal versus atherosclerotic arteries. A recombinant adenovirus including a nuclear-targeted beta-galactosidase gene was percutaneously delivered to the iliac artery of normal (n = 25) and atherosclerotic (n = 25) rabbits. Transgene expression, assessed by morphometric as well as chemiluminescent analyses, was documented in all normal and atherosclerotic arteries between 3 and 14 d after gene transfer, but was undetectable at later time points. Transfected cells were identified as smooth muscle cells located in the media of normal arteries, and in the neointima and the vasa-vasora of atherosclerotic arteries. Two percent of medial cells, but only 0.2% of medial and neointimal cells expressed the transgene in normal and atherosclerotic arteries, respectively (P = 0.0001). Similarly, nuclear beta-galactosidase activity was higher in normal than in atherosclerotic arteries (3.2 vs. 0.8 mU/mg protein, P = 0.02). These findings indicate that atherosclerosis reduces the transfection efficiency which can be achieved with adenoviral vectors, and thus constitutes a potential limitation to adenovirus-based, arterial gene therapy.

Effects of acute hyperoxic exposure on solute fluxes across the blood-gas barrier in rat lungs.

We investigated effects of acute hyperoxia on solute transport from air space to vascular space in isolated rat lungs. Air spaces were filled with Krebs-Ringer bicarbonate solution containing fluorescein isothiocyanate-labeled dextran (FD-20; mol wt 20,000) and either 22Na+ and [14C]sucrose, or D-[14C]glucose and L-[3H]glucose. Apparent permeability-surface area products for tracers over time (up to 120 min) were calculated for isolated perfused lungs from control rats (room air) and rats exposed to > 95% O2 for 48 or 60 h immediately postexposure. After O2 exposures, mean fluxes for [14C]sucrose and FD-20 were significantly higher than in room-air control lungs. However, amiloride-sensitive Na+ and active D-glucose fluxes were unchanged after hyperoxic exposure. Therefore, it is unlikely that decreases in net solute transport in this lung-injury model contributed to pulmonary edema resulting from O2 toxicity. Increased net solute transport shown to help resolve pulmonary edema after acute hyperoxic exposure must therefore begin during the recovery period. In summary, our data show increases in passive solute fluxes but no changes in active solute fluxes immediately after acute hyperoxic lung injury.

[Neutrophils and monocytes in gingival epithelium]

Neutrophils and monocytes of gingival epithellium in health gingiva(H),marginal gingivitis(MG),juvenile periodontitis(JP),adult periodontitis(AP) and subgingival bacteria were quantitated and analyzed,The results showed that the numbers of PMN within either pocket epithelium or oral gingival epithelium in JP were significantly lower than in AP and G.The amounts of PMN in AP were much larger than other three groups.Positive correlation between the number of PMN in sulcular pocket epitelium and the motile bacteri of subgingival plaque was demonstrated by correlation analysis.Monocytes mainly presented in deep pocket and junctional epithelum which were stained by NAE method,however very few Langhans cells were seen in these areas.

Mouse model of angiogenesis.

Neovascularization of ischemic muscle may be sufficient to preserve tissue integrity and/or function and may thus be considered to be therapeutic. The regulatory role of vascular endothelial growth factor (VEGF) in therapeutic angiogenesis was suggested by experiments in which exogenously administered VEGF was shown to augment collateral blood flow in animals and patients with experimentally induced hindlimb or myocardial ischemia. To address the possible contribution of postnatal endogenous VEGF expression to collateral vessel development in ischemia tissues, we developed a mouse model of hindlimb ischemia. The femoral artery of one hindlimb was ligated and excised. Laser Doppler perfusion imaging (LDPI) was employed to document the consequent reduction in hindlimb blood flow, which typically persisted for up to 7 days. Serial in vivo examinations by LDPI disclosed that hindlimb blood flow was progressively augmented over the course of 14 days, ultimately reaching a plateau between 21 and 28 days. Morphometric analysis of capillary density performed at the same time points selected for in vivo analysis of blood flow by LDPI confirmed that the histological sequence of neovascularization corresponded temporally to blood flow recovery detected in vivo. Endothelial cell proliferation was documented by immunostaining for bromodeoxyuridine injected 24 hours before each of these time points, providing additional evidence that angiogenesis constitutes the basis for improved collateral-dependent flow in this animal model. Neovascularization was shown to develop in association with augmented expression of VEGF mRNA and protein from skeletal myocytes as well as endothelial cells in the ischemic hindlimb; that such reparative angiogenesis is indeed dependent upon VEGF up-regulation was confirmed by impaired neovascularization after administration of a neutralizing VEGF antibody. Sequential characterization of the in vivo, histological, and molecular findings in this novel animal model thus document the role of VEGF as endogenous regulator of angiogenesis in the setting of tissue ischemia. Moreover, this murine model represents a potential means for studying the effects of gene targeting on nutrient angiogenesis in vivo.

Therapeutic angiogenesis following arterial gene transfer of vascular endothelial growth factor in a rabbit model of hindlimb ischemia.

The plasmid phVEGF165, expressing the 165-amino-acid isoform of vascular endothelial growth factor (VEGF), an endothelial cell specific mitogen, was applied to the polymer coating of an angioplasty balloon and delivered percutaneously to the iliac artery of rabbits in which the femoral artery had been excised to cause hindlimb ischemia. Site-specific transfection of phVEGF165 resulted in augmented development of collateral vessels documented by serial angiograms, and increased capillary density as well as increased capillary/myocyte ratio documented histochemically at necropsy. Consequent amelioration of the hemodynamic deficit in the ischemic limb was documented by improvement in the calf blood pressure ratio (ischemic/normal limb) to 0.70 +/- 0.08 in the VEGF-transfected group vs 0.50 +/- 0.18 in controls (p < 0.05). These findings suggest that site-specific arterial gene transfer of VEGF165 may achieve physiologically meaningful therapeutic modulation of vascular insufficiency.

Synergistic effect of vascular endothelial growth factor and basic fibroblast growth factor on angiogenesis in vivo.

BACKGROUND: Recent studies have suggested that vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF) may have synergistic effects on the induction of angiogenesis in vitro. Therefore, we investigated the hypothesis that the simultaneous administration of VEGF and bFGF, each having been previously shown to independently enhance collateral development in an animal model of hind limb ischemia, could have a synergistic effect in vivo. METHODS AND RESULTS: Ten days after surgical induction of unilateral hind limb ischemia, New Zealand White rabbits were randomized to receive either VEGF 500 micrograms alone (n = 6), bFGF 10 micrograms alone (n = 7), VEGF 500 micrograms, immediately followed by 10 micrograms bFGF (n = 7), or vehicle only (control animals, n = 8) in each case administered intra-arterially via a catheter in the internal iliac artery of the ischemic limb. BP ratio (BPR, ischemic/healthy limb) at day 10 for the VEGF+bFGF group was 0.82 +/- 0.01, much superior (P < .0005) to that of either the VEGF group (0.52 +/- 0.02) or the bFGF group (0.57 +/- 0.02). This outcome persisted at day 30: BPR in the VEGF+bFGF group (0.91 +/- 0.02) exceeded that of the control group (0.49 +/- 0.05, P < .0001), the VEGF group (0.65 +/- 0.03, P < .0005), or the bFGF group (0.66 +/- 0.03, P < .0005). Serial angiography demonstrated a progressive increase in luminal diameter of the stem collateral artery and the number of opacified collaterals in the thigh of the ischemic limbs in all groups. Stem artery diameter with VEGF+bFGF (1.34 +/- 0.07 mm) on day 30 was significantly (P < .05) greater than with either VEGF (1.09 +/- 0.09) or bFGF (1.18 +/- 0.06) alone. Capillary density was significantly greater (P < .05) in VEGF+bFGF animals (275 +/- 20 mm2) compared with VEGF (201 +/- 8) or bFGF (209 +/- 15). CONCLUSIONS: Combined administration of VEGF and bFGF stimulates significantly greater and more rapid augmentation of collateral circulation, resulting in superior hemodynamic improvement compared with either VEGF or bFGF alone. This synergism of two angiogenic mitogens with different target cell specificities may have important implications for the treatment of severe arterial insufficiency in patients whose disease is not amenable to direct revascularization.

Time course of increased cellular proliferation in collateral arteries after administration of vascular endothelial growth factor in a rabbit model of lower limb vascular insufficiency.

Proliferation of vascular cells has been previously shown to contribute to spontaneous development of coronary collaterals. Recent studies from several laboratories have established that collateral artery growth in both the heart and limb can be enhanced by administration of angiogenic growth factors, or therapeutic angiogenesis. In this study, we sought (1) to define the extent and time course of endothelial cell (EC) and smooth muscle cell (SMC) proliferation accompanying spontaneous collateral development during limb ischemia and (2) to determine the extent to which proliferative activity of ECs and SMCs is augmented during therapeutic angiogenesis with vascular endothelial growth factor (VEGF), a heparin-binding EC-specific mitogen. Ten days after induction of limb ischemia by surgically excising the femoral artery of rabbits, either VEGF (500 to 1000 micrograms) or saline was administered as a bolus into the iliac artery of the ischemic limb. Cellular proliferation was evaluated by bromodeoxyuridine labeling for 24 hours at day 0 (immediately before VEGF administration) and at days 3, 5, and 7 after VEGF, EC proliferation in the midzone collaterals of VEGF-treated animals increased 2.8-fold at day 5 (P < 0.05 versus control), and returned to baseline levels by day 7. SMC proliferation in midzone collaterals also increased 2.7-fold in response to VEGF (P < 0.05). No significant increase in EC or SMC proliferation was observed in either the stem or re-entry collaterals of VEGF-treated animals compared with untreated ischemic control animals. Reduction of hemodynamic deficit in the ischemic limb measured by lower limb blood pressure was documented at day 7 after VEGF (P < 0.01 versus untreated, ischemic control). These data thus (1) establish the contribution of cellular proliferation to collateral vessel development in limb ischemia and (2) support the concept that augmented cellular proliferation contributes to the enhanced formation of collateral vessels after therapeutic angiogenesis with VEGF.

Physiological assessment of augmented vascularity induced by VEGF in ischemic rabbit hindlimb.

This study was designed to assess the physiological consequences of augmented vascularity induced by administration of vascular endothelial growth factor (VEGF), an endothelial cell-specific mitogen, in a rabbit model of hindlimb ischemia. Ten days after excision of the common and superficial femoral arteries from one hindlimb of 24 New Zealand White rabbits, VEGF (n = 15) or saline (control; n = 9) was selectively injected into the ipsilateral internal iliac artery. Limb perfusion was evaluated immediately pre-VEGF (baseline) and again at days 10 and 30. A Doppler guide wire was advanced to the internal iliac artery to record flow velocity at rest and at maximum flow velocity provoked by intra-arterial injection of papaverine. At baseline and at day 10, no differences in flow parameters were observed between the control and the VEGF-treated animals. By day 30, however, flow at rest (P < 0.05), maximum flow velocity (P < 0.001), and maximum blood flow (P < 0.001) were all significantly higher in the VEGF-treated group. These physiological findings complement previous-anatomic studies by providing evidence that a single intra-arterial bolus of VEGF augments flow, particularly maximum flow, in the rabbit ischemic hindlimb. These data thus support the notion that VEGF administration represents a potential treatment strategy for certain patients with lower extremity ischemia.

Site-specific therapeutic angiogenesis after systemic administration of vascular endothelial growth factor.

PURPOSE: Recent experimental studies have established the feasibility of therapeutic angiogenesis; in all cases, this has been achieved with local administration of angiogenic growth factors. This study was designed to investigate the hypothesis that systemic administration of an angiogenic growth factor specifically mitogenic for endothelial cells--vascular endothelial growth factor (VEGF)--could augment collateral vessel development in a rabbit ischemic hindlimb model. METHODS: Ten days after the ligation of the external iliac artery and excision of the common and superficial femoral arteries in one limb of New Zealand white rabbits, heparin (800 IU, n = 13), VEGF (1 mg, n = 3; 5 mg, n = 5), heparin (800 IU) + VEGF (1 mg, n = 5; 5 mg, n = 7), or saline solution (n = 8) was injected as a single bolus in a marginal ear vein. Collateral vessel formation and limb perfusion were assessed 10 and 30 days after treatment. RESULTS: Animals in both VEGF-treated groups had a significantly higher (p < 0.01) increase in calf blood pressure ratio at day 10 (control, 0.44 +/- 0.02; heparin, 0.47 +/- 0.02; VEGF, 0.60 +/- 0.01; heparin+VEGF, 0.61 +/- 0.02) and day 30 (control, 0.49 +/- 0.05; heparin, 0.48 +/- 0.02; VEGF, 0.70 +/- 0.03; heparin+VEGF, 0.73 +/- 0.03). Both VEGF-treated groups had a significantly higher (p < 0.05) angiographic score at day 30 (control, 0.28 +/- 0.01; heparin, 0.28 +/- 0.01; VEGF, 0.37 +/- 0.01; heparin+VEGF, 0.38 +/- 0.02). Maximum flow reserve at day 30 in the ischemic limb was higher (p < 0.05) in VEGF-treated rabbits (control, 1.87 +/- 0.07; heparin, 1.92 +/- 0.08; VEGF, 2.42 +/- 0.16; heparin+VEGF, 2.33 +/- 0.12). Capillary density was higher (p < 0.01) in the ischemic muscles of VEGF-treated rabbits (control, 156 +/- 10/mm2; heparin, 178 +/- 8/mm2; VEGF, 230 +/- 10/mm2; heparin+VEGF, 233 +/- 8/mm2). CONCLUSIONS: This series of in vivo experiments demonstrates that intravenous administration of VEGF, with or without heparin, results in both anatomic and physiologic evidence of enhanced collateral vessel formation in the rabbit ischemic hindlimb. Single-bolus systemic administration of VEGF may be a feasible therapeutic strategy in patients with lower-extremity ischemia.

Recovery of disturbed endothelium-dependent flow in the collateral-perfused rabbit ischemic hindlimb after administration of vascular endothelial growth factor.

BACKGROUND: Disturbed endothelium-dependent blood flow has been shown to be a feature of native collateral vessels. Recent studies have shown that recombinant angiogenic growth factors augment collateral development in animal models of hindlimb ischemia. We therefore investigated the hypothesis that the administration of an angiogenic growth factor, in this case vascular endothelial growth factor (VEGF), may promote recovery of disturbed endothelium-dependent blood flow in a rabbit model of hindlimb ischemia. METHODS AND RESULTS: Ischemia was induced by ligation of the external iliac artery and excision of the femoral artery in one limb of New Zealand White rabbits (day 0). Flow velocity was measured using a Doppler guide wire at rest and after administration of serotonin and acetylcholine. Blood flow (in mL/min) was calculated assuming a circular lumen geometry. In untreated control animals with an ischemic limb, serotonin administered at day 10 or 40 produced a decrease in hindlimb blood flow (71 +/- 2% and 33 +/- 6% reduction from baseline, respectively); in contrast, among animals treated with a single 500-micrograms bolus dose of VEGF administered selectively into the internal iliac artery at day 10 and studied at day 40, serotonin produced an increase in flow (119 +/- 8% from baseline; P < .05 versus control animals). Acetylcholine induced only a moderate increase in flow in control animals (152 +/- 15% at day 10 and 177 +/- 14% at day 40) in contrast to a profound increase among VEGF-treated animals studied at day 40 (254 +/- 25%; P < .05 versus control animals). CONCLUSIONS: To our knowledge, these findings constitute the first demonstration of successful pharmacological modulation of disturbed endothelium-dependent flow in the arterial circulation subserved by collateral vessels. This physiological benefit complements previously reported anatomic findings suggesting a favorable impact of angiogenic growth factors on collateral-dependent limb ischemia.