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Biomedical subjects

Yan Xiong

Publications and source records attributed to Yan Xiong.

At least 37 records · Page 2Linked to original sources

[Study of apoptosis of peripheral blood mononuclear cells in patients with multiple organ dysfunction syndrome].

OBJECTIVE: To study apoptosis of peripheral blood mononuclear cells (PBMCs) in patients with multiple organ dysfunction syndrome (MODS) and its associated gene Bcl-2 and p53 expression. METHODS: Twenty-five patients with MODS and 18 healthy volunteers were enrolled for the study. Flow cytometry assay, electron microscopy, acridine orange-ethidium bromide staining and fluorescence microscopy, DNA agarose gel electrophoresis were used to identify and quantify apoptosis of PBMCs. Reverse transcription-polymerase chain reaction (RT-PCR) was used to quantify Bcl-2 mRNA and p53 mRNA expression. RESULTS: Typical morphological features of apoptotic PBMCs were observed in the patients. The apoptosis rate in MODS group was (25.4+/-9.2)%, and it was higher than that of control group (15.9+/-6.8)% (P<0.01). The number of apoptotic cells was (1.040+/-0.096)/high power field in MODS group, and it was higher than that in control group (0.235+/-0.028)/high power field (P<0.05). Bcl-2 mRNA expression of PBMCs in patients was significantly lower than that of healthy volunteers (0.11+/-0.09 vs. 0.19+/-0.06, P<0.05), while p53 mRNA expression was higher in patients than that of healthy volunteers (0.45+/-0.09 vs. 0.25+/-0.12, P<0.05). CONCLUSION: PBMCs apoptosis in patients with MODS is increased abnormally. The expression of Bcl-2 mRNA in patients is decreased while p53 mRNA expression is increased. The results suggest that abnormal apoptosis of monocytes as well as abnormal expression of apoptosis associated genes occur in patients with MODS.

Adult↗

[Experimental studies on decorin in suppression of postoperative flexor tendon adhesion in rabbits].

OBJECTIVE: To study the effect of decorin in the suppression of postoperative flexor tendon adhesion. METHODS: Eighteen Japanese large ear white rabbits underwent complete transection of the II digit flexor digitorum profundus tendon in zone I and defects immediately were repaired using the modified Kessler technique with 5-0 nonabsorbable monofilament suture. The site of the right repaired tendon was then injected with 100 microl of decorin (0.25 mg/ml) as test toe, the site of the left repaired tendon with 100 microl of PBS as control toe. In every group, rabbits were killed and the feet were prepared for biomechanical testing, macroscopic examination and histological inspection. RESULTS: In every group, biomechanical testing demonstrates that the sliding distances and the ranges of motion significantly increased in the test toe compared with the control toe (P < 0.05); macroscopic examination demonstrated that the tendon adhesions of the test toe were significantly reduced when compared with the control toe. In the tese toe, hematoxylin and eosin staining revealed that the hyperplasia of fibroblast was significantly delayed and the collagen fibrils arranged regularly and had the normal diameters. CONCLUSION: Decorin can significantly reduce the flexor tendon adhesion formation, adjust collagen fibrillogenesis and promote the tendon healing.

Animals↗

[Study of relationship between cyclooxygenase and platelet-activating factor on peripheral blood mononuclear cells in patients with systemic inflammatory response syndrome and multiple organ dysfunction syndrome].

OBJECTIVE: To study the role of cyclooxygenase (COX) and platelet-activating factor (PAF) in pathophysiologic mechanisms of patients with systemic inflammatory response syndrome (SIRS) and multiple organ dysfunction syndrome (MODS). METHODS: Twenty-eight adult patients whose diagnosis met American college of chest physicians/society of critical care medicine (ACCP/SCCM) criteria for SIRS and MODS were enrolled for study including 13 cases for SIRS group and 15 cases for MODS group. The normal control group consisted of 11 healthy volunteers who matched with study subjects for age and gender. Enzyme linked immunoadsorbent assay (ELISA) was used to measure the content of COX-2 and the activity of platelet-activating factor acetylhydrolase (PAF-AH) of peripheral blood mononuclear cells (PBMCs). Reverse transcription polymerase chain reaction (RT-PCR) was used to measure the COX-2 mRNA and PAF-AH mRNA expression of PBMCs. RESULTS: The content of COX-2 and the activity of PAF-AH of PBMCs and the expression of their mRNA in MODS group were higher than those in SIRS group and control group (all P<0.05). There was no significant difference between SIRS group and control group. The content of COX-2 and the activity of PAF-AH and the expression of their mRNA of PBMCs in non-survivors were higher than those in survived patients (all P<0.05). In 3 groups, positive correlation was found between the COX-2 content and PAF-AH activity (r=0.329, P<0.05). The leukocyte count, lymphocyte count, and PaO(2)/FiO(2) of peripheral blood in non-survivors showed no significant difference with those of survived patients (all P>0.05). The blood glucose and creatinine of non-survivors were higher than those of survived patients (P<0.05 and P<0.01). The total CO(2) content (TCO(2)) and pH value of non-survivors were lower than those of survived patients (both P<0.01). CONCLUSION: This study shows that COX-2 and PAF-AH play a role in the occurrence of MODS and they can be used as indexes to judge the prognosis of SIRS and MODS. Blood glucose, creatinine, TCO(2) and pH value of blood can be used as other indexes for judging the state and the prognosis of the illness.

1-Alkyl-2-acetylglycerophosphocholine Esterase↗

p38 Mitogen-activated protein kinase plays a stimulatory role in hepatic gluconeogenesis.

Hepatic gluconeogenesis is essential for maintaining blood glucose levels during fasting and is the major contributor to postprandial and fasting hyperglycemia in diabetes. Gluconeogenesis is a classic cAMP/protein kinase A-dependent process initiated by glucagon, which is elevated in the blood during fasting and in diabetes. In this study, we have shown that p38 mitogen-activated protein kinase (p38) was activated in liver by fasting and in primary hepatocytes by glucagon or forskolin. Fasting plasma glucose levels were reduced upon blockade of p38 with either a chemical inhibitor or small interference RNA in mice. In examining the mechanism, inhibition of p38 suppressed gluconeogenesis in liver, along with expression of key gluconeogenic genes, including phosphoenolpyruvate carboxykinase and glucose-6-phosphatase. Peroxisome proliferator-activated receptor gamma coactivator 1alpha and cAMP-response element-binding protein have been shown to be important mediators of hepatic gluconeogenesis. We have shown that inhibition of p38 prevented transcription of the PPARgamma coactivator 1alpha gene as well as phosphorylation of cAMP-response element-binding protein. Together, our results from in vitro and in vivo studies define a model in which cAMP-dependent activation of genes involved in gluconeogenesis is dependent upon the p38 pathway, thus adding a new player to our evolving understanding of this physiology.

Acetylcysteine↗

The heparin-binding site of antithrombin is crucial for antiangiogenic activity.

The heparin-binding site of antithrombin is shown here to play a crucial role in mediating the antiangiogenic activity of conformationally altered cleaved and latent forms of the serpin. Blocking the heparin-binding site of cleaved or latent antithrombin by complexation with a high-affinity heparin pentasaccharide abolished the serpin's ability to inhibit proliferation, migration, capillary-like tube formation, basic fibroblast growth factor (bFGF) signaling, and perlecan gene expression in bFGF-stimulated human umbilical vein endothelial cells. Mutation of key heparin binding residues, when combined with modifications of Asn-linked carbohydrate chains near the heparin-binding site, also could abrogate the anti-proliferative activity of the cleaved serpin. Surprisingly, mutation of Lys114, which blocks anticoagulant activation of antithrombin by heparin, caused the native protein to acquire antiproliferative activity without the need for conformational change. Together, these results indicate that the heparin-binding site of antithrombin is of crucial importance for mediating the serpin's antiangiogenic activity and that heparin activation of native antithrombin constitutes an antiangiogenic switch that is responsible for turning off the antiangiogenic activity of the native serpin.

Angiogenesis Inhibitors↗

Effect of diabetic duration on serum concentrations of endogenous inhibitor of nitric oxide synthase in patients and rats with diabetes.

This study was designed to investigate the effect of diabetic duration on serum concentrations of endogenous inhibitor of nitric oxide synthase N(G), N(G)-asymmetric dimethylarginine (ADMA) in patients and rats with diabetes, and to determine whether elevated endogenous ADMA is implicated in endothelial dysfunction or macroangiopathy in diabetes. Experimental diabetic model was induced by a single intraperitoneal injection of streptozotocin to male Sprague-Dawley rats and fed for 2-, 4- and 8-week, respectively. Type 2 diabetic patients with different diabetic duration were recruited from Xiangya Hospital. Plasma glucose and serum ADMA levels were measured in both patients and rats. Moreover, endothelium-dependent relaxation of thoracic aortas and some parameters of metabolic control were examined in rats. Serum ADMA concentrations were significantly elevated in type 2 diabetic patients compared with healthy subjects (3.44 +/- 0.40 vs 1.08 +/- 0.14 micromol/L, n = 50 in diabetic patients and n = 40 in healthy subjects, P < 0.01). The serum levels of ADMA in patients with macroangiopathy were higher than the patients without macroangiopathy (P < 0.01). But no difference was observed in serum ADMA concentrations between groups of patients with different diabetic duration. Similarly, serum levels of ADMA in diabetic rats were also significantly elevated at 2-week duration compared with duration-matched control (3.71 +/- 0.20 vs 1.04 +/- 0.23 micromol/L, n = 5 approximately 6, P < 0.01). This elevation of ADMA was retained to 4- and 8-week (3.54 +/- 0.76 vs 0.95 +/- 0.06 micromol/L for 4-week, 3.21 +/- 0.50 vs 1.03 +/- 0. 09 micromol/L for 8-week, n = 5 approximately 6, all P < 0.01) and remained unchanged among three diabetic groups. The elevation of ADMA was accompanied by impairment of endothelium-dependent relaxation and poor metabolic control in diabetic rat. These results first reveal that the extent of elevation in serum ADMA in both rats and patients with diabetes is not proportion with the length of their diabetic duration but rather with the metabolic control of this disease. Elevated endogenous ADMA may be implicated in diabetes-induced endothelial dysfunction and macroangiopathy. This study is helpful to prevention and treatment of diabetic-induced endothelial dysfunction or macroangiopathy.

Adult↗

A reduction of endogenous asymmetric dimethylarginine contributes to the effect of captopril on endothelial dysfunction induced by homocysteine in rats.

We examined whether captopril exerts beneficial effect on homocysteine-induced endothelial dysfunction in vivo and whether this effect of captopril is associated with a reduction of endogenous inhibitor of nitric oxide synthase (NOS) asymmetric dimethylarginine (ADMA) in rats. Male Sprague-Dawley rats were given intravenous injections of homocysteine (10 mg/kg/day) to induce endothelial dysfunction. Captopril treatment (3 mg/kg/day, i.v.) was taken in some rats after homocysteine administration. Endothelium-dependent relaxation was tested in aortic rings. Serum levels of ADMA, nitrite/nitrate, malondialdehyde (MDA), and creatinine were measured. Furthermore, superoxide dismutase activity in liver and angiotensin converting enzyme activity in serum were also assayed. Administration of homocysteine to rats for 4 weeks significantly impaired endothelium-dependent relaxation compared with control rats. This impairment of endothelium-dependent relaxation was accompanied by elevated serum concentration of ADMA and decreased serum content of nitrite/nitrate. Moreover, serum concentration of MDA was remarkably increased, whereas liver superoxide dismutase activity was decreased in homocysteine-treated group compared with control. Chronic captopril treatment not only improved the impaired endothelium-dependent relaxation, but also prevented the elevation of serum ADMA and MDA levels, as well as reduction of serum nitrite/nitrate contents and liver superoxide dismutase activity. Serum angiotensin converting enzyme activity and creatinine had no significant difference between the three groups. These results suggest that chronic captopril treatment reduces endogenous inhibitor of NOS in rats with homocysteine injection, which may contribute to the beneficial effect of captopril on homocysteine-induced endothelial dysfunction in vivo, and may be secondary to the antioxidative action of captopril.

Acetylcholine↗

Pravastatin restores DDAH activity and endothelium-dependent relaxation of rat aorta after exposure to glycated protein.

This study was designed to investigate whether glycated bovine serum albumin (AGE-BSA) inhibits dimethylarginine dimethylaminohydrolase (DDAH) activity to contribute to its adverse effect on endothelium-dependent relaxation in rat aorta, and whether pravastatin reverses the inhibition of DDAH activity and endothelial dysfunction induced by AGE-BSA. Endothelium-dependent relaxation of aortic rings was measured by isometric tension recording, and DDAH activity, and the contents of nitrite/nitrate as well as malondialdehyde (MDA) in aortic tissue were determined after exposure of Sprague-Dawley rat aorta to AGE-BSA (1.70 mmol/L) for 60 minutes in the presence or absence of pravastatin. In comparison with control, both endothelium-dependent relaxation and DDAH activity (0.032 +/- 0.002 versus 0.095 +/- 0.003 U/g protein, n = 5, P < 0.01) were significantly inhibited in isolated rat aorta after exposure to AGE-BSA, which was accompanied by decreases of nitrite/nitrate contents and elevations of MDA levels in aorta. Treatment with pravastatin (1 mmol/L) not only prevented the inhibition of endothelial function but also reversed the decrease of DDAH activity induced by AGE-BSA and normalized the alterations in nitrite/nitrate and MDA contents. Similar effects were observed when rat aorta exposed to AGE-BSA in the presence of antioxidant pyrrolidine dithiocharbamate (PDTC, 30 micromol/L) or protein kinase C inhibitor chelerythrine (1 micromol/L). These results suggested that decreased DDAH activity may be involved in endothelial dysfunction of rat aorta induced by AGE-BSA, and that pravastatin restores DDAH activity and endothelium-dependent relaxation after aorta exposure to AGE-BSA, which may be secondary to its antioxidative effects.

Amidohydrolases↗

Visualization of autophagy in Arabidopsis using the fluorescent dye monodansylcadaverine and a GFP-AtATG8e fusion protein.

Autophagy is a process that is thought to occur in all eukaryotes in which cells recycle cytoplasmic contents when subjected to environmental stress conditions or during certain stages of development. Upon induction of autophagy, double membrane-bound structures called autophagosomes engulf portions of the cytoplasm and transfer them to the vacuole or lysosome for degradation. In this study, we have characterized two potential markers for autophagy in plants, the fluorescent dye monodansylcadaverine (MDC) and a green fluorescent protein (GFP)-AtATG8e fusion protein, and propose that they both label autophagosomes in Arabidopsis. Both markers label the same small, apparently membrane-bound structures found in cells under conditions that are known to induce autophagy such as starvation and senescence. They are usually seen in the cytoplasm, but occasionally can be observed within the vacuole, consistent with a function in the transfer of cytoplasmic material into the vacuole for degradation. MDC-staining and the GFP-AtATG8e fusion protein can now be used as very effective tools to complement biochemical and genetic approaches to the study of autophagy in plant systems.

Arabidopsis↗

AtATG18a is required for the formation of autophagosomes during nutrient stress and senescence in Arabidopsis thaliana.

Vacuolar autophagy is a major pathway by which eukaryotic cells degrade macromolecules, either to remove damaged or unnecessary proteins, or to produce respiratory substrates and raw materials to survive periods of nutrient deficiency. During autophagy, a double membrane forms around cytoplasmic components to generate an autophagosome, which is transported to the vacuole. The outer membrane fuses with the vacuole or lysosome, and the inner membrane and its contents are degraded by vacuolar or lysosomal hydrolases. We have identified a small gene family in Arabidopsis thaliana, members of which show sequence similarity to the yeast autophagy gene ATG18. Members of the AtATG18 gene family are differentially expressed in response to different growth conditions, and one member of this family, AtATG18a, is induced both during sucrose and nitrogen starvation and during senescence. RNA interference was used to generate transgenic lines with reduced AtATG18a expression. These lines show hypersensitivity to sucrose and nitrogen starvation and premature senescence, both during natural senescence of leaves and in a detached leaf assay. Staining with the autophagosome-specific fluorescent dye monodansylcadaverine revealed that, unlike wild-type plants, AtATG18a RNA interference plants are unable to produce autophagosomes in response to starvation or senescence conditions. We conclude that the AtATG18a protein is likely to be required for autophagosome formation in Arabidopsis.

Arabidopsis↗

Effect of pravastatin on impaired endothelium-dependent relaxation induced by lysophosphatidylcholine in rat aorta.

AIM: To investigate the effects of pravastatin, a potent 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor, on impaired endothelium-dependent relaxation induced by lysophosphatidylcholine (LPC), the major component of oxidized low-density lipoprotein, in rat thoracic aorta. METHODS: Both the endothelium-dependent relaxation response to acetylcholine and the endothelium-independent relaxation response to sodium nitroprusside of aortic rings were measured by recording isometric tension after the rings were exposed to LPC in the absence or presence of pravastatin to estimate the injury effect of LPC and the protective effect of pravastatin on the aortic endothelium, respectively. RESULTS: Exposure of aortic rings to LPC (1-10 micromol/L) for 30 min induced a significant concentration-dependent inhibition of endothelium-dependent relaxation to acetylcholine, but did not affect endothelium-independent relaxation in response to sodium nitroprusside. Pre-incubation of aortic rings with pravastatin (0.3-3 mmol/L) for 15 min and then co-incubation of the rings with LPC (3 micromol/L) for another 30 min significantly attenuated the inhibition of endothelium-dependent relaxation induced by LPC. This protective effect of pravastatin (1 mmol/L) was abolished by NG-nitro-L-arginine methyl ester (30 micromol/L), an inhibitor of nitric oxide synthase, but not by indomethacin (10 micromol/L), an inhibitor of cyclooxygenase. Moreover, protein kinase C inhibitor chelerythrine (1 micromol/L) the superoxide anion scavenger superoxide dismutase (200 kU/L), and the nitric oxide precursor L-arginine (3 mmol/L) also improved the impaired endothelium-dependent relaxation induced by LPC, similar to the effects of pravastatin. CONCLUSION: Pravastatin can protect the endothelium against functional injury induced by LPC in rat aorta, a fact which is related to increasing nitric oxide bioavailability.

Alkaloids↗

Dynamic flight stability of a hovering bumblebee.

The longitudinal dynamic flight stability of a hovering bumblebee was studied using the method of computational fluid dynamics to compute the aerodynamic derivatives and the techniques of eigenvalue and eigenvector analysis for solving the equations of motion. For the longitudinal disturbed motion, three natural modes were identified: one unstable oscillatory mode, one stable fast subsidence mode and one stable slow subsidence mode. The unstable oscillatory mode consists of pitching and horizontal moving oscillations with negligible vertical motion. The period of the oscillations is 0.32 s (approx. 50 times the wingbeat period of the bumblebee). The oscillations double in amplitude in 0.1 s; coupling of nose-up pitching with forward horizontal motion (and nose-down pitching with backward horizontal motion) in this mode causes the instability. The stable fast subsidence mode consists of monotonic pitching and horizontal motions, which decay to half of the starting values in 0.024 s. The stable slow subsidence mode is mainly a monotonic descending (or ascending) motion, which decays to half of its starting value in 0.37 s. Due to the unstable oscillatory mode, the hovering flight of the bumblebee is dynamically unstable. However, the instability might not be a great problem to a bumblebee that tries to stay hovering: the time for the initial disturbances to double (0.1 s) is more than 15 times the wingbeat period (6.4 ms), and the bumblebee has plenty of time to adjust its wing motion before the disturbances grow large.

Animals↗

[Study on the changes in serum leukotrienes B4 and p38 mitogen activated protein kinase in multiple organ dysfunction syndrome].

OBJECTIVE: To investigate the changes in serum leukotrienes B4(LTB4) and p38 mitogen activated protein kinase (p38 MAPK) in multiple organ dysfunction syndrome (MODS) and to evaluate the relationship between LTB4 and p38 MAPK and clinical condition of patients with MODS. METHODS: The clinical condition of 26 patients with MODS was evaluated with scoring system. The serum LTB4 and p38 MAPK of the said patients and that of 12 healthy individuals were determined with enzyme linked immunoadsorbent assay(ELISA). The correlation of the scores of MODS and levels of serum LTB4 and p38 MAPK was analyzed. The correlation of the scores of MODS and levels of serum LTB4 and p38 MAPK was analyzed in non-survivors and survivors. RESULTS: The serum level of LTB4[(923.96+/-308.65)ng/L] was significantly lower in MODS patients compared with control group [(2 453.31+/-400.93)ng/L, P<0.05]. There was no significant difference in serum level of p38 MAPK between the patients with MODS [(193.83+/-106.32)ng/L]ls and control group [(124.36+/- 84.50)ng/L, P>0.05]. There was significant difference in the serum level of LTB4 between the survivors[(1 334.51+/-530.35)ng/L] and non-survivors [(444.98+/-206.30)ng/L, P<0.05]. There were significant negative correlations between serum LTB4 and MODS scores (P<0.001). CONCLUSION: The pathophysiological changes in later period of MODS are different from those of other common inflammatory responses. Serum LTB4 and p38 MAPK could be one of the indexes of the severity and prognosis on MODS.

Adolescent↗

[Changes of serum asymmetric dimethylarginine in essential hypertension before and after the treatment].

OBJECTIVE: To investigate the relationship between serum asymmetric dimethylarginine (ADMA) and blood pressure as well as target organ damage in essential hypertension, and to evaluate the effects of enalapril and losartan on them. METHODS: Forty-two newly diagnoszed patients with essential hypertension were randomly divided into enalapril-treated group and losartan-treated group. Serum ADMA, L-arginine, and nitric oxide( NO) were measured before and after the treatment for 8 weeks. Twenty-three healthy volunteers were included as control subjects. RESULTS: The concentrations of ADMA and L-arginine in serum were significantly higher but the level of nitric oxide was relatively lower ( P < 0.01 ) in hypertensive patients than those in control subjects. Serum ADMA was higher in different levels of blood pressure and target organ damage. Treatment with enalapril or losartan for 8 weeks not only reduced blood pressure but also decreased serum ADMA (P <0.01 ). Furthermore, treatment with these drugs also increased the level of serum nitric oxide but didn't change the level of L-arginine. CONCLUSION: The concentrations of serum ADMA and L-arginine were increased, but the level of nitric oxide was decreased in the early stage of essential hypertension. Both enalapril and losartan could ameliorate the endothelial function by reducing the concentration of ADMA.

Adult↗

Total knee replacement for posttraumatic degenerative arthritis of the knee.

OBJECTIVE: To evaluate the results of total knee arthroplasty (TKA) in patients with posttraumatic degenerative arthritis due to a previous fracture around the knee. METHODS: We analyzed the results of 15 TKAs, performed from 1997 to 2003, in 15 patients with post-traumatic degenerative arthritis due to a previous fracture around knee. There were 3 women and 12 men with an average age of 58 years (range, 31-76 years). The time from fracture to arthroplasty averaged 8.2 years (range, 2-27 years). Internal fixation had previously been performed in 8 patients resulting in retained hardware. At the time of arthroplasty a femoral fracture malunion was present in two knees. Lateral retinacular release (4 knees), extensor mechanism realignment (1 knee) or medial collateral ligament reconstruction (1 knee) were needed at the time of arthroplasty. RESULTS: Follow-up averaged 35 months (range, 12-73 months). No patient was lost for follow-up. According to the Knee Society Score scale, the mean preoperative knee score was 37 (range, 10-70) and functional score was 41 (range, 0-60). They were improved significantly to a mean of 84 (range, 10-100) and 76 (range, 20-100) points, respectively at the latest follow-up. The mean knee arc of motion were improved from 84 degree preoperation to 94 degree at the latest follow-up. Postoperative manipulation under anesthesia for poor motion was carried out in 4 knees. No knee had aseptic loosening that required subsequent revision. Two knees developed superficial infection and were treated with debridement. It subsequently recovered with the retention of components. CONCLUSIONS: Significant improvement in function and relief of pain has been achieved in patients with previous fractures undergoing subsequent TKA. However, this procedure is technically demanding and patients are at increased risk for restricted motion and need more care following TKA. This study suggests that the outcome of TKA may be improved further by making special efforts to restore limb alignment, to ensure correct component positioning, and to manage soft tissue balance.

Adult↗

Femoral component revision using extensively porous-coated cementless stem.

OBJECTIVE: To evaluate the clinical and radiographic results of extensively porous-coated femoral stem in revision of total hip arthroplasty (THA). METHODS: From January 1999 to December 2003, fifteen hips of fifteen cases received revision of THA with extensively porous-coated femoral stem. There were six males and nine females. The average age was 66 years (ranging 58-82 years). The reason for the revision was aseptic loosening in 10 cases, septic loosening in 2, femoral shaft fracture around loose implant in 2, and femoral revision for malposition of the femoral component in 1. All the patients were clinically evaluated using Harris hip score and radiographically evaluated both preoperatively and postoperatively at regular follow-up intervals. RESULTS: No patients were lost for follow-up. The average length of follow-up was 2.3 years (range, 1-5 years). The average preoperative Harris hip score was 42 points, which was improved to 89 points at latest follow-up. The latest follow-up showed that bone in-growth occurred in fourteen stems and solid fibrous fixation in one. Complications consisted of femoral shaft fracture in two cases (1 undisplaced distal femur fracture and 1 cortical perforation at the tip of the prosthesis), and postoperative dislocation in one. There was no mechanical failure of the stem in this study. CONCLUSIONS: Satisfactory results of short-term clinical and radiographic follow-up have been achieved in using extensively porous-coated femoral stem for revision of THA. It should be noticed that the straight, 203 mm stem should be used with caution in short people.

Journal Article↗

[Total hip arthroplasty with uncemented cup and femoral head autografts for coxarthrosis due to dysplasia].

OBJECTIVE: To evaluate the outcomes of total hip arthroplasty (THA) for coxarthrosis due to dysplasia with acetabular reconstruction of an uncemented cup in conjunction with a femoral head autograft. METHODS: A retrospective study was made on 21 hips in 20 patients (18 female and 2 male; average age, 50 years) with developmental hip dysplasia treated by THA with use of an uncemented cup. The acetabular cup was placed at the level of the true acetabulum; all patients required autogenous femoral head grafts due to acetabular deficiency. The average coverage of the acetabular cup by the femoral head autograft was 31% (range, 10% to 45%). Eight hips had less than 25% cup coverage and 13 between 25% and 50%. The average follow-up period was 4.7 years (range, 1-8 years). All patients were evaluated with the use of a modified Harris hip score. Radiographic evaluations were made by preoperative and follow-up. RESULTS: All autografts were seen to be united to host-bone. No collapse of the autograft and no hip had the evidence of loosening of component seen in all patients. According to the modified Harris hip score, the average hip score increased from 46 at preoperation to 89 at the final review. Preoperative leg-length discrepancy was greater than 2 cm seen in all except 1 patient with bilateral hip dysplasia. After surgery, only 2 of 20 patients still had a leg-length discrepancy greater than 1 cm. Three hips showed minor resorption in the lateral portion of the graft which was not supporting the cup. Three hips developed grade 1 Brooker heterotopic ossification and one had grade 2. CONCLUSIONS: THA with an uncemented cup in conjunction with a femoral head autograft for coxarthrosis due to dysplasia could obtain favorable results. This method could provide reliable acetabular fixation and appeared to restore acetabular bone stock in patients with developmental hip dysplasia when the coverage of the cementless cup by the graft does not exceed 50%.

Adult↗