Objective To evaluate the technique and clinical results of the modular fluted tapered stems for treating periprosthetic femoral fractures in revision hip arthroplasty.Methods From August 2007 to February 2014,fourteen patients (14hips) with periprosthetic femoral fractures underwent revision hip arthroplasty with modular fluted tapered stem.A retrospective analysis was performed involving all patients who were followed-up more than 2 years.The subjects consisted of 4 males and 10 females with mean age of 73.4±6.6 years (range,62-82 years) at the time of revision.All patients were unilateral with 8 left hips and 6 right hips.The status of primary arthroplasty was bipolar hemiarthroplasty in 3 patients and total hip arthroplasty in 11 patients.Nine cases were with cemented stems,5 cases with uncemented stems.The interval from primary hip arthroplasty to revision surgery ranged from 40 to 163 months,with an average of 120.9±31.9 months.Eight cases with Vancouver type B3 periprosthetic femoral fracture were found preoperatively,6 cases with aseptic loosening and bone deficiency occurred periprosthetic femoral fracture during the operation.Based on the Paprosky classification system for femoral bone deficiency:type ⅢA in 8 hips,type ⅢB in 5 hips,type Ⅳ in 1 hip.Both the femoral and the acetabular components were revised in 9 patients.All femoral fractures were treated with cable fixation,and the cortical allograft struts were used to augment femoral bone stock in 7 patients.The patients were followed up at 6 weeks,3 months,6 months,9 months,12 months and annually thereafter.Harris Hip Score System and radiographic examination was used to evaluate the clinical results,including fracture union,implant stability,bone stock,hip joint function and postoperative complications.Results The mean duration of follow-up was 62.1 ±22.2 months (range,30-96 months).The mean times of fracture union were 6.2±2.5 months (range,3-12 months).The Harris Hip Score improved from 29.6± 10.3 preoperatively to 86.3±4.2 postoperatively (t=-21.6,P=0.00).Thirteen cases (93％,13/14) had the stem subsidence of 4.9±2.5 mm (range,0-9 mm).Thirteen cases (93％,13/14) were presented with femoral bony restoration.Two cases showed incorporation of the allograft in 7 patients.One patient developed deep venous thrombosis of lower limbs,and one suffered from subcutaneous hematomas after surgery.There was no infection,aseptic loosening,dislocation or periprosthetic fracture complications at the followup.Conclusion The short-medium term results of the modular fluted tapered prosthesis applied in periprosthetic femoral fractures are encouraging in revision hip arthroplasty.The present technology can provide reliable primary stability and can tolerate minimal subsidence postoperatively.

In this study, we observed the levels of adrenomedullin (ADM) and proadrenomedullin N-terminal 20 peptide (PAMP) in myocardium and aorta of spontaneously hypertensive rats (SHRs) in comparison with Wistar-kyoto (WKY) rats. Contents of ADM and PAMP were measured by radioimmunoassay (RIA) in plasma, myocardium and aorta. The amount of Pro-ADM mRNA of myocardium and aorta was determined by competitive quantitative reverse transcription polymerase chain reaction (RT-PCR). In SHRs the amounts of Pro-ADM mRNA of myocardium and aorta were 66.7% (P<0.01) and 73% (P<0.01) higher than those in WKY rat, respectively. In SHRs, the levels of ADM in plasma, myocardium and aorta were 29%, 76.7% and 79% (all P<0.01) higher than those in WKY rats, respectively. The level of PAMP in SHRs was increased by 42.5% in plasma (P<0.01), 47.2% in myocardium (P<0.0.1) and 27.3% in aorta (P<0.05) compared to WKY rats, respectively. In addition, the ratio of ADM content to PAMP content in SHRs group was increased compared with that in WKY group (2.0+/-0.25 vs 1.64+/-0.3 and 2.2+/-0.18 vs 1.56+/-0.28, in myocardium and aorta, respectively, P<0.01). These results suggest that ProADM gene expression is up-regulated and the increase in ADM and PAMP is different in SHRs. The significance of inconsistency of increase in ADM and PAMP in SHRs needs to be further investigated.
Adrenomedullin ; genetics ; metabolism ; Animals ; Aorta ; metabolism ; Female ; Male ; Myocardium ; metabolism ; RNA, Messenger ; genetics ; metabolism ; Rats ; Rats, Inbred SHR ; Rats, Inbred WKY ; Up-Regulation

AIM AND METHODSTo observe the effect of myocardial mitochondrial L-arginine (L-Arg)/nitric oxide (NO) system on mitochondrial Ca2+ transport by using purified rat mitochondria and incubation of them in vitro.

RESULTSCompared with control group, incubation of mitochondria with L-Arg (10(-4) mol/L, NO substrate) or sodium nitroprusside (5 x 10(-7) mol/L, the donor of exogenous NO, SNP) increased significantly mitochondrial NO2- (66% and 89%, P < 0.01), respectively, and decreased the Ca2+ content (40% and 54%, P < 0.01). After L-Arg or SNP treatment, mitochondrial Ca2+ uptake were decreased by 67% and 85%, respectively (P < 0.01), vs control. The rate of mitochondrial Ca2+ release decreased by 11% and 8%, respectively (P < 0.01). When L-NAME (NO synthase inhibitor) was incubated with mitochondria and the L-Arg together, it inhibited the effects of L-Arg, NO2 on the mitochondrial NO2 formation, Ca2+ content descending, and decrease of Ca2+ uptake and release.

CONCLUSIONThe data suggest that myocardial mitochondrial L-Arg /NO systems take part in the regulation of cardiomyocytes Ca2+ transportation.

Animals ; Arginine ; metabolism ; Biological Transport ; Calcium ; metabolism ; Female ; Male ; Mitochondria, Heart ; metabolism ; Myocytes, Cardiac ; metabolism ; Nitric Oxide ; metabolism ; Nitric Oxide Synthase ; metabolism ; Rats ; Rats, Wistar

AIMThe characteristics of ryanodine receptor in rat cardiac sarcoplasmic reticulum (SR) and nuclear envelope (NE) were studied.

METHODSVelocity and isopyknic gradient centrifugation was employed to fractionate rat SR and NE. Ryanodine receptor was assayed with [3H] ryanodine saturate binding to the preparations.

RESULTSThe maximal binding (Bmax) and dissociating constant (Kd) of ryanodine receptor in rat cardiac NE were, 1.7% and 60% of those in SR respectively. Phosphorylation in vitro by PKA and PKC increased Bmax of the receptors in SR by 372% and 121%, and augmented those in NE by 221% and 306%, without any effects on Kd.

CONCLUSIONRyanodine receptors were present in rat myocardial NE, with lower density and higher affinity than those located in SR, which can be activated by PKA and PKC.

Animals ; Calcium ; metabolism ; Kinetics ; Myocardium ; metabolism ; Nuclear Envelope ; metabolism ; physiology ; Phosphorylation ; Rats ; Rats, Sprague-Dawley ; Ryanodine ; metabolism ; Ryanodine Receptor Calcium Release Channel ; metabolism ; Sarcoplasmic Reticulum ; metabolism ; physiology

BACKGROUNDHuman urotensin II (UII) is the most potent mammalian vasoconstrictor identified so far. Our previous study showed that UII is a potent mitogen of airway smooth muscle cells (ASMC) inducing ASMC proliferation in a dose-dependent manner. The signal transduction pathway of UII mitogenic effect remains to be clarified. This study was conducted to investigate the signal transduction pathway in the proliferation of ASMC induced by UII.

METHODSIn primary cultures of rat ASMCs, activities of protein kinase C (PKC), mitogen-activated protein kinase (MAPK) and calcineurin (CaN) induced by UII were measured. The effect of CaN on PKC and MAPK was studied by adding cyclosporin A (CsA), a specific inhibitor of CaN. Using H7 and PD98059, inhibitors of PKC and MAPK, respectively, to study the effect of PKC and MAPK on CaN. The cytosolic free calcium concentration induced by UII was measured using Fura-2/AM.

RESULTSUII 10(-7) mol/L stimulated ASMC PKC and MAPK activities by 44% and 24% (P < 0.01), respectively, after incubating for 20 minutes. It increased CaN activity in a time-dependent manner, being 1.68 times as that of control for 24 hours (P < 0.01). It promoted the cytosolic free calcium concentration increase of 18% (P < 0.01). CsA 10(-6) mol/L and H7 50 micromol/L inhibited UII-stimulated CaN activity by 45% (P < 0.01) and 21% (P < 0.05), respectively, while PD98059 50 micromol/L had no effect on CaN activity (P > 0.05). CsA 10(-6) mol/L inhibited UII-stimulated PKC activity by 14% (P < 0.05), while having no effect on MAPK activity (P > 0.05).

CONCLUSIONSUII increases cytosolic free calcium concentration and activates PKC, MAPK and CaN. The signal transduction pathway between PKC and CaN has cross-talk.

Animals ; Calcineurin ; metabolism ; Cells, Cultured ; Enzyme Activation ; Mitogen-Activated Protein Kinases ; metabolism ; Mitogens ; pharmacology ; Myocytes, Smooth Muscle ; cytology ; Protein Kinase C ; metabolism ; Rats ; Signal Transduction ; physiology ; Trachea ; cytology ; Urotensins ; pharmacology

The change in plasma ghrelin level after 4-and 12-week adjunctive therapy of rosiglitazones in type 2 diabetic patients inadequately controlled by sulphonylurea alone was observed and the relation between ghrelin and insulin resistance was analysed.The results showed that rosiglitazones significantly increased circulating ghrelin level and obviously decreased insulin resistance index after therapy for 4 and 12 weeks in type 2 diabetic patients.

AIMTo investigate the alterations of taurine transport, and taurine transporter (TAUT) mRNA by hyperglycemia in cultured rat cardiomyocytes.

METHODS3H-taurine measured the amount of taurine uptake. TAUT mRNA consents were measured using quantitative RT-PCR.

RESULTSThe cellular uptake amounts of taurine in seven groups increased with incubation time, and near to be saturated after 5 min. The uptake amount of 10, 20, and 30 mmol/L glucose groups was obviously lower than that of the control group (P < 0.05 or P < 0.01). In 30 mmmol/L glucose, taurine release obviously was decreased, as compared with that of the control. Exposure of cells to 10, 20, and 30 mmmol/L glucose decreased taurine uptake in a concentration-dependent fashion. Exposure to hyperglycemia did not affect the Km of the TAUT, but the apparent Vmax were significantly decreased (P < 0.05). In 20 and 30 mmmol/L groups, TAUT mRNA contents of myocardial cells were significantly reduced, as compared with the control group (P < 0.05).

CONCLUSIONThe data suggests that there are dysfunction of taurine uptake and downregulation of TAUT gene expression by glucose in cultured rat cardiomyocytes.

Animals ; Cells, Cultured ; Glucose ; pharmacology ; Hyperglycemia ; metabolism ; Membrane Glycoproteins ; genetics ; metabolism ; Membrane Transport Proteins ; genetics ; metabolism ; Myocytes, Cardiac ; drug effects ; metabolism ; RNA, Messenger ; genetics ; Rats ; Rats, Sprague-Dawley ; Taurine ; metabolism

The present study investigated the contribution of endogenous heme oxygenase (HO)/carbon monoxide (CO) system to hypertension pathogenesis of rats. Zinc deuteroporphyrin 2,4-bisglycol (ZnDPBG),an inhibitor of heme oxygenase (HO), was used to inhibit HO activity in vivo. It was found that the blood pressure of rats with HO inhibition was significantly elevated, and plasma levels of adrenaline, noradrenaline,endothelin, nitrate and nitrite were significantly increased. HO activity and HbCO formation within vascular smooth muscle tissues were significantly inhibited after administration of ZnDPBG. Furthermore, administration of exogenous CO into HO inhibiting rats led to MABP decrease, but injection of HO substrate, heme-Llysinate, had no effect on HO inhibition-induced hypertension. In spontaneously hypertensive rats, injection of exogenous CO resulted in a significant decrease of MABP, and heme-L-lystnate had a similar effect with exogenous CO. These data show that HO/CO system has an anti-hypertension biological action, suggesting that endogenous CO plays an important role in hypertension pathogenesis.

A sepsis model induced by cecal ligation and puncture was used to study the role of endogenous carbon monoxide in hypotension pathogenesis of rats during septic shock. After administration of zinc deuteroporphyrin 2,4-bisglycol (ZnDPBG),an inhibitor of heme oxygenase (HO),blood pressure (BP),HO activity and carbon monoxide (CO) release from vascular muscle tissue were measured. The results showed that BP of sepsis rats,including systolic and diastolic arterial BP,decreased significantly while HO activity and CO content were significantly increased. In contrast,after administration of ZnDPBG,BP of sepsis rats was significantly increased while the HO activity and CO production were significantly decreased. These findings suggest that HO activity and CO release within vascular musculature are increased during septic shock;inhibition of HO may elevate BP of rats during septic shock through a decrease of endogenous CO production. It is concluded that endogenous CO derived from vascular muscle cells plays an important role in regulating vascular tone,and the up-regulation of HO activity followed by subsequent CO production contributes to hypotension pathogenesis during septic shock.

The purpose of the present study was to explore the expression changes of intermedin/adrenomedullin 2 (IMD/ADM2), a novel small molecular bioactive peptide, and its receptors, calcitonin receptor-like receptor (CRLR) and receptor activity modifying proteins (RAMP1, RAMP2, RAMP3) in the right ventricle of rats with chronic hypoxia-induced pulmonary hypertension. Twenty male Sprague-Dawley rats were randomly divided into 4-week hypoxia group and normal control group (each n=10). The rats in hypoxia group were placed in an isobaric hypoxic chamber, in which O(2) content was maintained at 9%-11% by delivering N(2), and CO(2) content was maintained at <3% for 4 weeks (8 h/d, 6 d/week). The rats in the control group were housed in room air. The protein levels of IMD/ADM2 and adrenomedullin (ADM) in blood plasma and right ventricular tissue were measured by radioimmunoassay. The mRNA expressions of IMD/ADM2, ADM and their receptors CRLR, RAMP1, RAMP2, RAMP3 in right ventricular tissue were determined by reverse transcription-polymerase chain reaction (RT-PCR). The results showed that the ratio of right ventricle weight to left ventricle plus septum weight [RV/(LV+S)] and mean pulmonary arterial pressure (mPAP) were higher in hypoxia group than those in the control group (all P<0.01), suggesting that the rat model of pulmonary hypertension was successfully established. However, the mean carotid arterial pressure (mCAP) between the two groups had no significant difference. Compared with that in the control group, ADM contents in plasma and right ventricular tissue in hypoxia group increased by 1.26 and 1.68 folds (all P<0.01), respectively. Likewise, IMD/ADM2 contents in blood plasma and right ventricular tissue in hypoxia group increased by 0.90 and 1.19 folds (P<0.01), respectively, compared with that in the control group. The data of RT-PCR showed that mRNA levels of ADM, IMD/ADM2 and RAMP2 in hypoxia group increased by 155.1% (P<0.01), 80.9% (P<0.01) and 52.9% (P<0.05), respectively, compared with those in the control group. There were no significant differences in mRNA expressions of CRLR, RAMP1 and RAMP3 between the two groups (all P>0.05). Taken together, the results show that the level of IMD/ADM2 increases in the rats with chronic hypoxia-induced pulmonary hypertension.
Adrenomedullin ; metabolism ; Animals ; Calcitonin Receptor-Like Protein ; metabolism ; Heart Ventricles ; metabolism ; Hypertension, Pulmonary ; etiology ; metabolism ; physiopathology ; Hypoxia ; complications ; Male ; Neuropeptides ; metabolism ; Rats ; Rats, Sprague-Dawley ; Receptor Activity-Modifying Proteins ; metabolism