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Biomedical subjects

J Y Su

Publications and source records attributed to J Y Su.

At least 19 recordsLinked to original sources

Total knee arthroplasty after failed dome osteotomy.

A retrospective, clinical and radiographic analysis was done between a study group of 15 patients with 17 total knee arthroplasties done following failed, proximal-tibial dome osteotomies and a control group of 14 patients with 17 primary arthroplasties. The groups were matched according to age of patients, type of prosthesis, primary disease and length of follow-up. The average length of follow-up was 59.4 months (range, 25-146 mo) in the study group and 62.3 months (range, 43-140 mo) in the control group. On the basis of the knee rating scale of the American Knee Society, 94% of the patients had either an excellent or a good result in the study group. There were no significant differences in knee scores, function scores, or range of motion of the knee between the two groups during the follow-up period. Although two overcorrected valgus knees and one severe varus knee necessitated an autogeneic bone graft for tibial defects at the time of implantation of the secondary prosthesis, dome osteotomy does not appear to compromise a subsequent arthroplasty.

Aged↗

Adult monteggia fracture with ipsilateral distal radius fracture: case report.

Although the adult Monteggia fracture is a well-known injury, the combination of a Monteggia fracture and an ipsilateral distal radius fracture is extremely rare. It is important for the treating physician to recognize that this injury involves not only the bone elements but also their articulations. The distortion of the integrity of both the elbow and the wrist results in the potential for functional compromise, if inadequately treated. The case report presented here describes a 21-year-old woman with this complex injury resulting from a fall. The injury included a Monteggia type II fracture and an ipsilateral distal radius intra-articular fracture in the left forearm. An excellent result was obtained by surgical intervention in both the radial and ulnar bones. The factors we believe contributed to the excellent result were early diagnosis, anatomic reduction, stable fixation, and early physical exercise. The mechanism of injury giving rise to this rare combination of fractures is discussed, as well as a review of the literature.

Adult↗

MicroStructured Omnifit acetabular components: concerns with locking system complications and excessive polyethylene wear.

BACKGROUND: We began to use cementless MicroStructured Omnifit acetabular components in November 1988. Liner dislodging and excessive polyethylene wear later occurred in some of our patients. This finding prompted us to review our experience with the use of such modular acetabular components. METHODS: A total of 887 hips in 672 patients, which had been fitted with cementless MicroStructured Omnifit acetabular components, were evaluated for locking system complications using radiographic examinations. Of the cases, 240 hips which had received a 26-mm femoral head (group 1) and 110 hips which had received a 32-mm femoral head (group 2) were compared using a digitiser to determine the influence of femoral head size on polyethylene wear. RESULTS: There were two types of radiographic signs of locking system complications in 7 hips, at a mean time of 2.9 years after implantation. The incidence of liner locking system complications using this modular acetabular component was 0.8%. The mean liner wear rate per year was 0.15 mm in group 1 and 0.20 mm in group 2 (p <0.005). The initial polyethylene thickness ranged from 5.9 to 13.6 mm in group 1, compared with 3.9 to 10.6 mm in group 2 (p < 0.005). CONCLUSION: A patient who has received a total hip arthroplasty that includes a MicroStructured Omnifit acetabular component should be monitored frequently for radiographic signs of locking system complications. In this study, the mean liner wear rate was significantly higher in group 2. Inadequate polyethylene thickness in this group was implicated as the major cause of excessive polyethylene wear.

Adolescent↗

Reduction of H2O2-evoked, intracellular calcium increases in the rat N18-RE-105 neuronal cell line by pretreatment with an electrophilic antioxidant inducer.

Pretreatment of the neuronal cell line N18-RE-105 with the antioxidant enzyme inducer dimethyl fumarate (DMF) reduced cell death elicited by H2O2 (50 mM for 1 h) as measured 24 h after H2O2 washout. Oxidants like H2O2 may contribute to cell death by increasing intracellular ionized calcium ([Ca2+]i), suggesting that DMF may in part confer protection by altering H2O2-induced [Ca2+]i signals. To examine this possibility, we measured [Ca2+]i of fura-2-loaded cultures of DMF- and vehicle-pretreated cells during H2O2 superfusion. H2O2 exposure induced a delayed [Ca2+]i increase that was significantly lower in DMF-pretreated cells than controls. Elevation of extracellular cystine also reduced the H2O2 induced [Ca2+]i elevation. Thus, antioxidant upregulation may contribute to protection during oxidative stress by stabilizing [Ca2+]i. However, since oxidative stress may induce cytotoxicity by multiple pathways, [Ca2+]i stabilization may not be the only mechanism responsible for the protective effect of DMF.

Animals↗

Knee dislocation: treatment of high-velocity knee dislocation.

BACKGROUND: We report the outcomes of patients treated with a new arthroscopic treatment modality for knee dislocation after high-velocity trauma. METHODS: Twenty-three patients (12 men, 11 women; 25 knees) with traumatic knee dislocation were treated with this technique. Under arthroscopy with gravity inflow irrigation, the ruptured posterior cruciate ligament was reconstructed with a patellar bone-tendon-bone graft, and the anterior cruciate ligament was debrided subacutely. The collateral ligament, meniscus, and capsules were repaired through additional incisions. RESULTS: The average interval between injury and surgery was 11.1+/-5 days (range, 5 to 25 days). After a mean follow-up period of 27.2+/-7.86 months, the mean extension was 1+/-2 degrees and the average flexion was 129.6+/-4.91 degrees. The mean Lysholm score was 84. There were no major complications. CONCLUSION: Arthroscopic posterior cruciate ligament reconstruction seems to be an effective treatment for traumatic knee dislocation.

Adolescent↗

The influence of the gap size on the interfacial union between the bone and the tendon.

An in-vivo model of New Zealand white rabbit was used to study the influence of gap size on the interfacial union between bone and tendon through histological observation and mechanical testing. In the model, the anterior cruciate ligament (ACL) was cut and reconstructed by autografted semitendinosus tendon (with average diameter of 1.48 mm +/- 0.12 mm). Mechanical testing of the interfacial healing tissue was done on the 15th post-operative day. At that time the mean maximal tensile strength was 2.511 +/- 0.293 kg to a bone tunnel size of 1.5 mm. The maximal tensile strength lowered to 1.853 +/- 0.563 kg to a bone tunnel size of 1.8 mm. The maximal tensile strength lowered to 1.302 +/- 0.657 kg to a bone tunnel size of 2.0 mm. Using a paired-t test, the gap size was found to have great influence on the tensile strength of the interfacial healing tissue (p < 0.05). The histological study showed that the interfacial gap was connected by the new growing collagen fibers. The healing tissue appeared much denser and much more maturated and organized in the smaller interfacial gap in comparison with specimens with a larger gap so that it can tolerate higher tensile strength. From this study, we concluded that the gap size really plays an important role in the process of maturation and organization of interfacial healing tissue. Furthermore, we recommend that in order to achieve greater anchoring strength of the grafted tendons, the bone tunnel should be made with approximately the same diameter of grafted tendon.

Animals↗

Anterior knee pain after intramedullary tibial nailing.

BACKGROUND: Currently, intramedullary nailing is a well-accepted method for treating tibial shaft fractures, but some patients complain of anterior knee pain after surgery. Multiple factors may influence this troublesome complication. METHODS: This was a retrospective analysis of the medical records of 200 patients who were treated with intramedullary nailing after tibial shaft fractures. Sixty-four patients complained of knee pain after surgery. We evaluated the knee pain in relation to the surgical approach, radiographic readings, and the type of nail used. RESULTS: Among the 64 patients, 45 (70%) received central approaches and 19 (30%) received paramedial approaches (p = 0.0002); 46 patients (72%) showed nail protrusions on radiographs and only 18 patients (28%) were without nail impingement (p = 0.0001). Forty-three patients (67%) received Kuntscher nail fixation and just 21 patients (33%) had interlocking nail fixation (p = 0.0015). CONCLUSION: The use of the central patellar tendon splitted approach, nail protrusion observed on radiographs, and the insertion of a non-locking intramedullary nail were all significant risk factors for anterior knee pain after surgery. All these risk factors should be avoided in tibial nailing to decrease the problem of postoperative knee pain.

Fracture Fixation, Intramedullary↗

[The role of endogenous CO in the regulation of endothelin-induced VSMC proliferation and MAPK activity].

Heme oxygenase (HO) is a rate-limiting enzyme of heme degradation, which converts the cellular heme to bilirubin and carbon monoxide (CO). Recently it is suggested that endogenous CO plays an important role in regulating vascular tone under both physiological and pathological conditions, but it is not clear whether endogenous HO/CO system regulates vascular smooth muscle cell (VSMC) proliferation. In the present study, VMSC 3H-TdR incorporation, mitogen-activated protein kinase (MAPK) activity, HO activity and CO release were determined to study the role of endogenous HO/CO system in regulating the VSMC proliferation induced by endothelin-1 (ET-1) in a cultured system. The results showed that ET-1 increased VSMC 3H-TdR incorporation, MAPK activity, HO activity, and CO release were up-regulated. Pretreatment of HO inhibitor, zinc protoporphyrin-9 (ZnPP-9), increased the ET-1-induced VSMC 3H-TdR incorporation and MAPK activity by 31.8% and 36.6% (P < 0.01, respectively), whereas pretreatment of heme-L-lysinate (HLL), a HO substrate, inhibited these activities. This study demonstrated that up-regulation of VSMC endogenous HO represents a cellular protective response to stress or injury. Inhibition of HO may enhance VSMC proliferation induced by ET-1 in vitro, suggesting that endogenous HO/CO system may be directly involved in the regulation of VSMC proliferation through MAPK signaling pathway.

Animals↗

Role of endogenous carbon monoxide in the pathogenesis of hypotension during septic shock.

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.

Animals↗

Effects of halothane on the sarcoplasmic reticulum Ca2+ stores and contractile proteins in rabbit pulmonary arteries.

BACKGROUND: The authors' purpose of this study was to elucidate the mechanisms of direct effects of halothane on the contractile proteins and Ca2+ release from the sarcoplasmic reticulum Ca2+ stores using isolated skinned strips (sarcolemma permealized with saponin) from rabbit pulmonary arteries. METHODS: The sarcoplasmic reticular Ca2+ stores were examined by immersing the skinned strips sequentially in solutions to load Ca2+ into and release Ca2+ from the sarcoplasmic reticulum using caffeine, inositol 1,4,5-trisphosphate, or halothane. The contractile proteins were assessed by activating the strips with Ca2+ followed by administration of halothane (with or without protein kinase C inhibitors). Tension, fura-2 fluorescence activated by Ca2+ release, and phosphorylation of myosin light chains were measured. RESULTS: Halothane (0.07-3.00%) increased Ca2+, tension, and phosphorylation of myosin light chains in a dose-dependent manner. Halothane decreased accumulation of Ca2+ in the sarcoplasmic reticulum and enhanced the caffeine-induced tension transients. In strips pretreated with caffeine or inositol 1,4,5-trisphosphate, halothane-induced tension transients were reduced but Ca2+ was not. In strips activated by 1 microM Ca2+, halothane (0.5-3.0%) decreased 20-45% of the activated force at 15 min. Halothane (3%) transiently increased the force (20%) associated with increases in Ca2+ and phosphorylation of myosin light chains. The increased force was abolished and the subsequent relaxation was enhanced by the protein kinase C inhibitor bisindolylmaleimide but not by indolocarbazole Gö-6976. CONCLUSIONS: In skinned pulmonary arterial strips, halothane, at clinical concentrations, inhibits uptake of Ca2+ by and induces release of Ca2+ from intracellular stores possibly shared by caffeine and inositol 1,4,5-trisphosphate, which are regulated by phosphorylation of myosin light chains. The time-dependent inhibition of the contractile proteins by halothane may be mediated by Ca2+-independent protein kinase C.

Anesthetics, Inhalation↗

Mechanisms of isoflurane-increased submaximum Ca2+-activated force in rabbit skinned femoral arterial strips.

BACKGROUND: Isoflurane enhances contraction in isolated intact arterial rings by a protein kinase C (PKC) activator and also causes contracture in skinned arterial strips. This study investigated the mechanisms of this isoflurane activation of the contractile proteins of skinned strips. METHODS: The skinned strips, mounted on photodiode force transducers, were prepared from rabbit femoral arteries treated with saponin. The strips were activated by 1 microM Ca2+ (buffered with 7 mM EGTA) with or without inhibitors for PKC and calmodulin-dependent protein kinase II (CaM kinase II). When force reached steady state, isoflurane was administered and changes in force were observed. Another group of the strips was frozen to assay myosin light chain phosphorylation (MLC-p) using two-dimensional electrophoresis and immunoblotting. Analysis of variance was used to compare the results from test and control groups. Probability values <0.05 were significant. RESULTS: Isoflurane (1-5%) dose dependently increased (24-81%) the Ca2+-activated force. At 1% and 5% isoflurane, MLC-p did not change either as the force increased or reached a new steady state level. However, with 3% isoflurane, MLC-p transiently decreased (29.1% and 17.1% of total MLC for 0% and 3% isoflurane, respectively). The 3% isoflurane-increased force was blocked by 10 microM bisindolymaleidmide, an inhibitor of PKC, but not by 10 microM Gö-6976, an inhibitor of Ca2+-dependent PKC, and was enhanced 50% by 0.1 mM KN-62, an inhibitor of CaM kinase II. CONCLUSIONS: Isoflurane increased submaximum Ca2+-activated force in skinned femoral arterial strips by activating Ca2+-independent PKC, possibly epsilon isoezyme. The isoflurane-decreased MLC-p may be caused by activation of CaM kinase II.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗

Inhibitory effect of trapidil on proliferation of cultured rat aortic smooth muscle cells induced by endothelin-1.

AIM: To study the effect of trapidil (Tra) on endothelin-1-induced proliferation of cultured rat aortic vascular smooth muscle cells (VSMC). METHODS: The [3H]TdR incorporation into DNA assay, the number of VSMC, and cell cycle distribution were measured. RESULTS: Pretreated with endothelin-1 100 nmol.L-1, cell number, [3H]TdR uptake, and cell mitogenic activity increased 134% +/- 23%, 210% +/- 70%, and 86% +/- 18%, respectively. This proliferation was inhibited by Tra 5, 50, 500 mumol.L-1. The inhibitory rates were 12%-48%, 35%-54% and 15%-47%, respectively. Tra did not influence the proliferation of VSMC without endothelin-1 pretreatment. CONCLUSION: Tra antagonized the proliferation of VSMC induced by endothelin-1.

Animals↗

[Effect of Arg-Gly-Asp-Ser (RGDS) peptide on ADP-induced signal transduction of activated rat platelet].

The purpose of this work was to investigate the effect of Arg-Gly-Asp-Ser (RGDS) peptide on platelet aggregation, protein phosphorylation, protein kinase C (PKC) and mitogen-activated protein kinase (MAPK) activity during platelet activation. Experiments were performed on ADP activated rat platelets in vivo. Results showed that 50 mumol/L ADP, in addition to inducing platelet aggregation, obviously enhanced not only PKC and MAPK activities but also 95 and 66 kD protein phosphorylation. When platelets and ADP were incubated together with 50, 100, 200 mumol/L RGDS peptide it was found that the latter markedly inhibited ADP activated platelet aggregation and activation of PKC and MAPK, both in a concentration-dependently manner. RGDS peptide also inhibited 95 and 66 kD protein phosphorylation concentration-dependently and went positively with its activation of PKC and MAPK. The above result suggested that the antithrombotic effect of RGDS peptide was probably mediated through its effect on intracellular signal transduction in the ADP activation of platelets.

Adenosine Diphosphate↗

Role of endogenous carbon monoxide in hypertension pathogenesis of rats.

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-L-lysinate, 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-lysinate 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.

6-Ketoprostaglandin F1 alpha↗

Efficient enzymatic synthesis of 13C,15N-labeled DNA for NMR studies.

The power of heteronuclear NMR spectroscopy to study macromolecules and their complexes has been amply demonstrated over the last decade. The obstacle to routinely applying these techniques to the study of DNA has been the synthesis of 13C,15N-labeled DNA. Here we present a simple and efficient method to generate isotope-labeled DNA for NMR studies that is as easy as that for isotope labeling of RNA. The method was used to synthesize a uniformly 13C,15N-labeled 32-nucleotide DNA that binds to human basic fibroblast growth factor with high affinity and specificity. Isotope-edited experiments were applied to the 13C,15N-labeled DNA bound to unlabeled protein, and the 13C,15N-labeled DNA was also examined in complex with 15N-labeled protein. The NMR experiments show that the DNA adopts a well-defined stable structure when bound to the protein, and illustrate the potential of 13C,15N-labeled DNA for structural studies of DNA-protein complexes.

Carbon Isotopes↗

Effects of recombinant human endothelial-derived interleukin-8 on hemorrhagic shock in rats.

AIM: To study the effects of recombinant human endothelial-derived interleukin-8 (IL-8) on hemorrhagic shock. METHODS: A profound hemorrhagic shock in rats was produced by exsanguination from femoral artery with mean arterial blood pressure (MABP) maintained at 5.32 kPa for 90 min. After transfusion, IL-8 250 micrograms.kg-1 was i.v. injected. Plasma endothelin-1 (ET-1) and 6 ketoprostaglandin F1 alpha (6-KPGF1 alpha) contents were determined with radioimmunoassay. RESULTS: After i.v. IL-8, the MABP in IL-8 group was elevated obviously (P < 0.01), the rat survival 2 h after infusion was increased (P < 0.05). During profound shock the plasma ET-1 levels were higher (21 +/- 4 vs 8.2 +/- 1.8 ng.L-1, P < 0.01) and the plasma 6-KPGF1 alpha contents lower than those in normal rats (107 +/- 12 vs 157 +/- 11 ng.L-1, P < 0.01). IL-8 remarkably reduced the plasma ET-1 levels (10 +/- 4 ng.L-1, P < 0.01) and enhanced plasma 6-KPGF1 alpha contents (368 +/- 16 ng.L-1, P < 0.01). CONCLUSION: IL-8 has beneficial antishock effects.

6-Ketoprostaglandin F1 alpha↗

[L-arginine transport in cultured vascular smooth muscle cells of spontaneously hypertensive rats and effect of liposome on the transport].

The characteristics of L-arginine (L-Arg) transport in cultured aortic smooth muscle cells (SMC) of spontaneously hypertensive rat (SHR) and control WKY rats were studied and the effect of liposome as L-Arg carrier on the transport was investigated. The results showed that the L-Arg transport of SMC in SHR was obviously lower than that in WKY rats. Maximum transport velocity (Vmax) of high and low affinity in SHR were respectively 48% (P < 0.01) and 49% (P < 0.01) of WKY rat, while the michaelis constant (K(m)) showed no significant difference (P > 0.05). Increase of L-Arg transport induced by tumor necrosis factor-alpha (TNF alpha) in SMC of SHR was obviously lower than that in WKY rats (P < 0.01). The uptake of L-Arg increased 10 to 20 times in SMC when incubated with liposome encapsulated L-Arg (Liposome-L-Arg) than with free L-Arg. The transport velocity in SMC incubated with liposome-L-Arg showed no significant difference in SHR and WKY rats (P > 0.05). The transport of liposome-L-Arg in SMC was not affected by TNF alpha in both the types of rats. The above results indicate that there exists a functional disturbance in L-Arg transport in the SMC of SHR, but the L-Arg transport in SMC can be obviously enhanced when liposome is used as L-Arg carrier. Thus, it appears that liposome-L-Arg may have clinical perspective in the treatment of hypertension.

Animals↗