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Biomedical subjects

Hong Gao

Publications and source records attributed to Hong Gao.

At least 37 records · Page 2Linked to original sources

[Effects of glutamine on matrix metalloproteinase-3 and tissue inhibitor of metalloproteinase-3 expressions in myocardium of rats with sepsis].

OBJECTIVE: The underlying mechanisms for cardiac dysfunction in sepsis include the inhibitory effect of endotoxin and inflammatory factors on myocardium and the decrease in cardiac myocardial cells in number. However, whether there is ventricular remodeling resulted from the abnormalities of extracellular collagen metabolism and whether glutamine (Gln) can protect myocardium from LPS-induced damage as in reperfusion are unknown. The aim of the present study was to examine the effects of Gln on the expressions of matrix metalloproteinase-3 (MMP-3), tissue inhibitor of metalloproteinase-3 (TIMP-3) and their mRNA in myocardium of rats with sepsis. METHODS: Classical rat model of sepsis was established by intraperitoneal injection of lipopolysaccharide (LPS) (4 mg/kg, from Escherichia coli O(55): B(5), Sigma). from 121 Wistar rats aged 18 days were divided into three groups randomly, 0 h control group (normal saline: 1 ml/kg, n = 11), LPS group (LPS: 4 mg/kg, n = 55) and Gln group (LPS: 4 mg/kg and immediately 13.64% glutamine 1 ml/kg, Fresenus, n = 55). Furthermore, LPS and Gln groups were examined at 2 h, 4 h, 6 h, 24 h and 72 h time points (n = 11). On each time point, rats of LPS and Gln groups as well as control group were anesthetized with 1% chloral hydrate injected intraperitoneally at a dosage of 1 ml/kg. Then, rats were sacrificed, and the hearts were isolated. Eight of them were frozen at minus 80 degrees C to measure the expression of TIMP-3 mRNA by using RT-PCR. The expressions of MMP-3 and TIMP-3 were observed with immunohistochemistry and the expression of MMP-3 mRNA was observed by using in situ hybridization. RESULTS: (1) Compared to 0 h, the mRNA expressions of MMP-3 and TIMP-3 in LPS group significantly increased (P < 0.01) with the peak at 6 - 24 h. While, in Gln group, they were significantly higher than those in controls but significantly lower than those in LPS group with the peak at 24 h (P < 0.01). Even at 72 h, they were still higher than those at 0 h (P < 0.05 and P < 0.01). (2) Compared to 0 h, the expressions of MMP-3 and TIMP-3 in LPS group were significantly lower at any other time point with the lowest at 6 h (P < 0.01). In Gln group, these expressions were also significantly lower than those in controls, but significantly higher than those in LPS group with the lowest being postponed to 24 h (P < 0.01). (3) The ultra structure changed obviously. Z line was unclear and the ridge of mitochondrion disappeared. While, in Gln group, the myocardial injury was slight compared to that in LPS group. CONCLUSIONS: MMP-3 mRNA expression was increased and TIMP-3 mRNA expression was depressed in LPS-induced sepsis. Myocardial extracellular matrix was damaged in sepsis. Glutamine might decrease the effects of LPS on MMP-3 and TIMP-3 expressions and postpone the time of myocardial matrix injury.

Animals↗

103Pd radioactive stent inhibits biliary duct restenosis and reduces smooth muscle actin expression during duct healing in dogs.

BACKGROUND: This study was designed to assess the expression of smooth muscle actin (SMA) in the healing process after implanting a (103)Pd radioactive stent in the biliary duct, and to discuss the function and significance of this stent in preventing biliary stricture formation. METHODS: A model of biliary injury in dogs was made and then a (103)Pd radioactive stent was positioned in the biliary duct. The expression and distribution of SMA were assessed in the anastomotic tissue 30 days after implantation of the stent. RESULTS: SMA expression was less in the (103)Pd stent group than in the ordinary stent group. The (103)Pd stent inhibited scar contracture and anastomotic stenosis. CONCLUSION: The (103)Pd stent can reduce the expression of SMA in the healing process and inhibit scar contracture and anastomotic stenosis in the dog biliary duct.

Actins↗

[Effect of glutamine on apoptosis of the small intestine in young rats with endotoxemia and its mechanism].

OBJECTIVE: To study the effect of glutamine on intestinal epithelial apoptosis by examining changes regarding Bcl-2 and Bax mRNA expressions in the small intestine of young rats with endotoxemia and to explore the protective mechanism that glutamine may have. METHODS: A total of 120 18-day-old rats were randomly assigned into Endotoxemia, Glutamine-treated and Control groups (n = 40 each). The endotoxemia model was established by intraperitoneal injection of endotoxin (4 mg/kg of O55B5 Escherichia coli lipopolysaccharide). Rats in the Glutamine-treated group were intraperitoneally injected with N (2)-L-alanyl-L-glutamine (2 g/kg) along with endotoxin. Rats in the Control group were intraperitoneally injected with an equal volume of normal saline. The entire ileum was collected at 2, 4, 6, 24, and 72 hrs after injection. Bcl-2 and Bax mRNA expressions were detected by semi-quantities reverse transcriptase chain reaction. RESULTS: Bcl-2 mRNA was not expressed in the Control and the Endotoxemia groups but increased in the Glutamine-treated group at each time point. Bax mRNA expression was weak in the Control group, and significantly increased in the Endotoxemia group at each time point. The Glutamine-treated group showed noticeably reduced Bax mRNA expression at 2 hrs post-injection while other time points were similar to the Control group. The ratio of Bax and Bcl-2 mRNA expression at each time point in the Endotoxemia group was significantly higher than that in the Control group while the Glutamine-treated group demonstrated significantly lower ratio of Bax and Bcl-2 mRNA expression than both. CONCLUSIONS: Glutamine treatment increased Bcl-2 mRNA expression and decreased Bax mRNA expression, as a result, the ratio of Bax and Bcl-2 mRNA expression decreased. The effects of glutamine resulted in a suppression of intestinal epithelial apoptosis and maintained the integrity of the gut barrier structure.

Animals↗

Beta-blockers to prevent gastroesophageal varices in patients with cirrhosis.

BACKGROUND: Nonselective beta-adrenergic blockers decrease portal pressure and prevent variceal hemorrhage. Their effectiveness in preventing varices is unknown. METHODS: We randomly assigned 213 patients with cirrhosis and portal hypertension (minimal hepatic venous pressure gradient [HVPG] of 6 mm Hg) to receive timolol, a nonselective beta-blocker (108 patients), or placebo (105 patients). The primary end point was the development of gastroesophageal varices or variceal hemorrhage. Endoscopy and HVPG measurements were repeated yearly. RESULTS: During a median follow-up of 54.9 months, the rate of the primary end point did not differ significantly between the timolol group and the placebo group (39 percent and 40 percent, respectively; P=0.89), nor were there significant differences in the rates of ascites, encephalopathy, liver transplantation, or death. Serious adverse events were more common among patients in the timolol group than among those in the placebo group (18 percent vs. 6 percent, P=0.006). Varices developed less frequently among patients with a baseline HVPG of less than 10 mm Hg and among those in whom the HVPG decreased by more than 10 percent at one year and more frequently among those in whom the HVPG increased by more than 10 percent at one year. CONCLUSIONS: Nonselective beta-blockers are ineffective in preventing varices in unselected patients with cirrhosis and portal hypertension and are associated with an increased number of adverse events. (ClinicalTrials.gov number, NCT00006398.)

Adrenergic beta-Antagonists↗

Investigation of the iron-sulfur cluster in Mycobacterium tuberculosis APS reductase: implications for substrate binding and catalysis.

The sulfur assimilation pathway is a key metabolic system in prokaryotes that is required for production of cysteine and cofactors such as coenzyme A. In the first step of the pathway, APS reductase catalyzes the reduction of adenosine 5'-phosphosulfate (APS) to adenosine 5'-phosphate (AMP) and sulfite with reducing equivalents from the protein cofactor, thioredoxin. The primary sequence of APS reductase is distinguished by a conserved iron-sulfur cluster motif, -CC-X( approximately )(80)-CXXC-. Of the sequence motifs that are associated with 4Fe-4S centers, the cysteine dyad is atypical and has generated discussion with respect to coordination as well as the cluster's larger functional significance. Herein, we have used biochemical, spectroscopic, and mass spectrometry analysis to investigate the iron-sulfur cluster and its role in the mechanism of Mycobacterium tuberculosis APS reductase. Site-directed mutagenesis of any cysteine residue within the conserved motif led to a loss of cluster with a concomitant loss in catalytic activity, while secondary structure was preserved. Studies of 4Fe-4S cluster stability and cysteine reactivity in the presence and absence of substrates, and in the free enzyme versus the covalent enzyme-intermediate (E-Cys-S-SO(3)(-)), suggest a structural rearrangement that occurs during the catalytic cycle. Taken together, these results demonstrate that the active site functionally communicates with the iron-sulfur cluster and also suggest a functional significance for the cysteine dyad in promoting site differentiation within the 4Fe-4S cluster.

Adenosine Monophosphate↗

Preparation, characterization, and application of multistimuli-responsive microspheres with fluorescence-labeled magnetic cores and thermoresponsive shells.

Novel functional microspheres with multistimuli-responsive properties have been prepared and characterized. The as-prepared microspheres respond to an external magnetic field, environmental temperature, and ultraviolet radiation. The in vitro drug-loading efficiency and drug-release behavior of these microspheres demonstrated that they could be used as drug carriers for drug controlled release. The results of in vivo distribution investigations of these microspheres showed that they exhibit a high magnetic-targeting effect, which holds promise for applications in various fields such as magnetic drug targeting and tissue labeling, among others.

Journal Article↗

Mechanism and kinetics of metalloenzyme phosphomannose isomerase: measurement of dissociation constants and effect of zinc binding using ESI-FTICR mass spectrometry.

Electrospray ionization Fourier transform ion cyclotron resonance (ESI-FTICR) mass spectrometry was used to study the noncovalent complexation of a metalloenzyme, phosphomannose isomerase (PMI), which catalyzes the interconversion of mannose 6-phosphate and fructose 6-phosphate. The zinc cofactor binding effect and the noncovalent interactions of the holoenzyme with its two natural substrates and two inhibitors, erythrose 4-phosphate and mannitol 1-phosphate, were investigated. Under nondenaturing conditions, the intact zinc-containing monomeric protein ions were reproducibly observed with no dissociation. Molecular ions corresponding to apo-PMI monomer were obtained by dialyzing the holoenzyme against EDTA. The binding/release of the metal ion did not alter the charge-state distributions of the protein to any significant extent, but changed the binding affinity of the substrates by at least 5-fold. Using ESI-FTICR mass spectrometry, the binding stoichiometry and specificity of the enzyme-substrate and enzyme-inhibitor complexes were directly determined. The first time report of the apparent dissociation constant for the isomeric substrates of PMI was measured to be 88.8 microM. The relative dissociation constant of the two inhibitors derived from gas-phase noncovalent complexation was very similar to the relative inhibition constant derived from solution phase kinetics.

Enzyme Inhibitors↗

Hepatic peroxisomal fatty acid beta-oxidation is regulated by liver X receptor alpha.

Peroxisomes are the exclusive site for the beta-oxidation of very-long-chain fatty acids of more than 20 carbons in length (VLCFAs). Although the bulk of dietary long-chain fatty acids are oxidized in the mitochondria, VLCFAs cannot be catabolized in mitochondria and must be shortened first by peroxisomal beta-oxidation. The regulation of peroxisomal, mitochondrial, and microsomal fatty acid oxidation systems in liver is mediated principally by peroxisome proliferator-activated receptor alpha (PPARalpha). In this study we provide evidence that the liver X receptor (LXR) regulates the expression of the genetic program for peroxisomal beta-oxidation in liver. The genes encoding the three enzymes of the classic peroxisomal beta-oxidation cycle, acyl-coenzyme A (acyl-CoA) oxidase, enoyl-CoA hydratase/L-3-hydroxyacyl-CoA dehydrogenase, and 3-ketoacyl-CoA thiolase, are activated by the LXR ligand, T0901317. Accordingly, administration of T0901317 in mice promoted a dose-dependent and greater than 2-fold increase in the rate of peroxisomal beta-oxidation in the liver. The LXR effect is independent of PPARalpha, because T0901317-induced peroxisomal beta-oxidation in the liver of PPARalpha-null mice. Interestingly, T0901317-induced peroxisomal beta-oxidation is dependent on the LXRalpha isoform, but not the LXRbeta isoform. We propose that induction of peroxisomal beta-oxidation by LXR agonists may serve as a counterregulatory mechanism for responding to the hypertriglyceridemia and liver steatosis that is promoted by potent LXR agonists in vivo; however, additional studies are warranted.

Acetyl-CoA C-Acyltransferase↗

A conserved mechanism for sulfonucleotide reduction.

Sulfonucleotide reductases are a diverse family of enzymes that catalyze the first committed step of reductive sulfur assimilation. In this reaction, activated sulfate in the context of adenosine-5'-phosphosulfate (APS) or 3'-phosphoadenosine 5'-phosphosulfate (PAPS) is converted to sulfite with reducing equivalents from thioredoxin. The sulfite generated in this reaction is utilized in bacteria and plants for the eventual production of essential biomolecules such as cysteine and coenzyme A. Humans do not possess a homologous metabolic pathway, and thus, these enzymes represent attractive targets for therapeutic intervention. Here we studied the mechanism of sulfonucleotide reduction by APS reductase from the human pathogen Mycobacterium tuberculosis, using a combination of mass spectrometry and biochemical approaches. The results support the hypothesis of a two-step mechanism in which the sulfonucleotide first undergoes rapid nucleophilic attack to form an enzyme-thiosulfonate (E-Cys-S-SO(3-)) intermediate. Sulfite is then released in a thioredoxin-dependent manner. Other sulfonucleotide reductases from structurally divergent subclasses appear to use the same mechanism, suggesting that this family of enzymes has evolved from a common ancestor.

Adenosine Phosphosulfate↗

A crucial role of angiotensin converting enzyme 2 (ACE2) in SARS coronavirus-induced lung injury.

During several months of 2003, a newly identified illness termed severe acute respiratory syndrome (SARS) spread rapidly through the world. A new coronavirus (SARS-CoV) was identified as the SARS pathogen, which triggered severe pneumonia and acute, often lethal, lung failure. Moreover, among infected individuals influenza such as the Spanish flu and the emergence of new respiratory disease viruses have caused high lethality resulting from acute lung failure. In cell lines, angiotensin-converting enzyme 2 (ACE2) has been identified as a potential SARS-CoV receptor. The high lethality of SARS-CoV infections, its enormous economic and social impact, fears of renewed outbreaks as well as the potential misuse of such viruses as biologic weapons make it paramount to understand the pathogenesis of SARS-CoV. Here we provide the first genetic proof that ACE2 is a crucial SARS-CoV receptor in vivo. SARS-CoV infections and the Spike protein of the SARS-CoV reduce ACE2 expression. Notably, injection of SARS-CoV Spike into mice worsens acute lung failure in vivo that can be attenuated by blocking the renin-angiotensin pathway. These results provide a molecular explanation why SARS-CoV infections cause severe and often lethal lung failure and suggest a rational therapy for SARS and possibly other respiratory disease viruses.

Analysis of Variance↗

Kinetic measurements and mechanism determination of Stf0 sulfotransferase using mass spectrometry.

Mycobacterial carbohydrate sulfotransferase Stf0 catalyzes the sulfuryl group transfer from 3'-phosphoadenosine-5'-phosphosulfate (PAPS) to trehalose. The sulfation of trehalose is required for the biosynthesis of sulfolipid-1, the most abundant sulfated metabolite found in Mycobacterium tuberculosis. In this paper, an efficient enzyme kinetics assay for Stf0 using electrospray ionization (ESI) mass spectrometry is presented. The kinetic constants of Stf0 were measured, and the catalytic mechanism of the sulfuryl group transfer reaction was investigated in initial rate kinetics and product inhibition experiments. In addition, Fourier transform ion cyclotron resonance (FT-ICR) mass spectrometry was employed to detect the noncovalent complexes, the Stf0-PAPS and Stf0-trehalose binary complexes, and a Stf0-3'-phosphoadenosine 5'-phosphate-trehalose ternary complex. The results from our study strongly suggest a rapid equilibrium random sequential Bi-Bi mechanism for Stf0 with formation of a ternary complex intermediate. In this mechanism, PAPS and trehalose bind and their products are released in random fashion. To our knowledge, this is the first detailed mechanistic data reported for Stf0, which further demonstrates the power of mass spectrometry in elucidating the reaction pathway and catalytic mechanism of promising enzymatic systems.

Adenosine Diphosphate↗

Pooling samples within microarray studies: a comparative analysis of rat liver transcription response to prototypical toxicants.

Combining or pooling individual samples when carrying out transcript profiling using microarrays is a fairly common means to reduce both the cost and complexity of data analysis. However, pooling does not allow for statistical comparison of changes between samples and can result in a loss of information. Because a rigorous comparison of the identified expression changes from the two approaches has not been reported, we compared the results for hepatic transcript profiles from pooled vs. individual samples. Hepatic transcript profiles from a single-dose time-course rat study in response to the prototypical toxicants clofibrate, diethylhexylphthalate, and valproic acid were evaluated. Approximately 50% more transcript expression changes were observed in the individual (statistical) analysis compared with the pooled analysis. While the majority of these changes were less than twofold in magnitude ( approximately 80%), a substantial number were greater than twofold (approximately 20%). Transcript changes unique to the individual analysis were confirmed by quantitative RT-PCR, while all the changes unique to the pooled analysis did not confirm. The individual analysis identified more hits per biological pathway than the pooled approach. Many of the transcripts identified by the individual analysis were novel findings and may contribute to a better understanding of molecular mechanisms of these compounds. Furthermore, having individual animal data provided the opportunity to correlate changes in transcript expression to phenotypes (i.e., histology) observed in toxicology studies. The two approaches were similar when clustering methods were used despite the large difference in the absolute number of transcripts changed. In summary, pooling reduced resource requirements substantially, but the individual approach enabled statistical analysis that identified more gene expression changes to evaluate mechanisms of toxicity. An individual animal approach becomes more valuable when the overall expression response is subtle and/or when associating expression data to variable phenotypic responses.

Animals↗

Chromic-P32 phosphate treatment of implanted pancreatic carcinoma: mechanism involved.

AIM: To study the effects of chromic-P32 phosphate (32P colloids) interstitial administration in Pc-3 implanted pancreatic carcinoma, and investigate its anticancer mechanism. METHODS: Ninety-eight tumor bearing nude mice were killed at different time points after the injection of 32P colloids to the tumor core with observed radioactivity. The light microscopy, transmission electron microscopy (TEM) and immuno-histochemistry and flow cytometry were used to study the rates of tumor cell necrosis, proliferating cell nuclear antigen index, the micro vessel density (MVD). The changes of the biological response to the lymphatic transported 32P colloids in the inguinal lymph node (ILN) were dynamically observed, and the percentage of tumor cell apoptosis, and Apo2.7, caspase-3, Bcl-2, Bax-related gene expression were observed too. RESULTS: The half-life of effective medication is 13 d after injection of 32P colloids to the tumor stroma, in 1-6 groups, the tumor cell necrosis rates were 20%, 45%, 65%, 70%, 95% and 4%, respectively (F = 4.14-105.36, P<0.01). MVD were 38.5+/-4.0, 28.0+/-2.9, 17.0+/-2.9, 8.8+/-1.5, 5.7+/-2.3 and 65.0+/-5.2 (t = 11.9-26.1, P<0.01), respectively. Under TEM fairly differentiated Pc-3 cells were found. Thirty days after medication, tumors were shrunk and dried with scabs detached, and those in control group increased in size prominently with plenty of hypodermic blood vessels. In all animals the ILN were enlarged but in medicated animals they appeared later and smaller than those in control group. The extent of irradiative injury in ILN was positively correlated to the dosage of medication. Typical tumor cell apoptosis could be found under TEM in animals with intra-tumoral injection of low dosed 32P colloids. The peak of apoptosis occurred in 2.96 MBq group and 24 h after irradiation. In the course of irradiation-induced apoptosis, the value of Bcl-2/Bax was down regulated; Apo2.7 and caspase-3 protein expression were prominently increased dose dependently. CONCLUSION: 32P colloids intra-tumor injection having prominent anticancer effectiveness may reveal the ability of promoting cell differentiation. The low dose 32P colloids may induce human pancreatic carcinoma Pc-3 implanted tumor cell apoptosis; Apo2.7, caspase-3, Bcl-2 and Bax protein participated in regulating the process of irradiation induced cell apoptosis.

Animals↗

Preparation and characterization of SARS in-house reference antiserum.

A reference antiserum for SARS is in urgent need in the development of SARS vaccine and other serological test of SARS research. Convalescent serum was collected from clinical confirmed patient. ELISA, Western-blotting and neutralization assay detected specific antibody against SARS coronavirus. This antiserum was prepared as in-house reference antiserum, freeze-dried and sealed in ampoules. The potency of this reference antiserum is defined to be 52.7 U after extensive calibration. Further, collaborative studies for the evaluation of this serum are needed in order to satisfy the requirements for international reference antiserum.

Animals↗

alpha-Glucosidase inhibition of 6-hydroxyflavones. Part 3: Synthesis and evaluation of 2,3,4-trihydroxybenzoyl-containing flavonoid analogs and 6-aminoflavones as alpha-glucosidase inhibitors.

The SAR studies suggested that the C-ring of baicalein (1) was not necessary for the activity, and validated the importance of 2,3,4-trihydroxybenzoyl structure of 1. Thus, a series of 2,3,4-trihydroxybenzoyl-containing flavonoid analogs were investigated for the alpha-glucosidase inhibitory activity. The results indicated that 5,6,7-trihydroxy-2-phenyl-4-quinolone (2) and 5,6,7-trihydroxyflavanone (4) showed the comparable activity to 1, while 3,5,6,7-tetrahydroxyflavone (7), 5,6,7-trihydroxyisoflavone (8), and 6-hydroxygenistein (9) showed moderate alpha-glucosidase inhibitory activity. In addition, it was found that 6-amino-5,7-dihydroxyflavone (16) was a more potent and specific rat intestinal alpha-glucosidase inhibitor than 1, and showed the comparable activity to acarbose. This is the first report on mammalian intestinal alpha-glucosidase inhibitory activity of 6-aminoflavones. Kinetic studies revealed that 16 inhibited both sucrose- and maltose-hydrolyzing activities of rat intestinal alpha-glucosidase uncompetitively.

Animals↗

A serological survey on neutralizing antibody titer of SARS convalescent sera.

A seroepidemiologic study was conducted in North China in 2003 to determine the neutralizing antibody titer of severe acute respiratory syndrome (SARS) convalescent sera. A total of 99 SARS convalescent serum samples were collected from patients from the Inner Mongolia Autonomous Region, Hebei Province, and Beijing 35-180 days after the onset of symptoms. The anti-SARS antibodies were detected by enzyme-linked immunosorbent assay (ELISA), neutralization assay, and Western blot. Eighty-seven serum samples were confirmed to be positive for SARS antibodies. The neutralizing antibody titer of the 87 positive sera was analyzed quantitatively by neutralization assay. The geometric mean titer (GMT) of the 87 convalescent sera was 1:61. The Kolmogorov-Smirnov test showed that the neutralizing antibody titers conform to normal distribution, which suggests that the average anti-SARS antibody level in this study was representative of the convalescent antibody level of the SARS population. This result could be useful for the development and quality control of SARS vaccines.

Antibodies, Viral↗

An animal model of SARS produced by infection of Macaca mulatta with SARS coronavirus.

A new SARS animal model was established by inoculating SARS coronavirus (SARS-CoV) into rhesus macaques (Macaca mulatta) through the nasal cavity. Pathological pulmonary changes were successively detected on days 5-60 after virus inoculation. All eight animals showed a transient fever 2-3 days after inoculation. Immunological, molecular biological, and pathological studies support the establishment of this SARS animal model. Firstly, SARS-CoV-specific IgGs were detected in the sera of macaques from 11 to 60 days after inoculation. Secondly, SARS-CoV RNA could be detected in pharyngeal swab samples using nested RT-PCR in all infected animals from 5 days after virus inoculation. Finally, histopathological changes of interstitial pneumonia were found in the lungs during the 60 days after viral inoculation: these changes were less marked at later time points, indicating that an active healing process together with resolution of an acute inflammatory response was taking place in these animals. This animal model should provide insight into the mechanisms of SARS-CoV-related pulmonary disease and greatly facilitate the development of vaccines and therapeutics against SARS.

Animals↗

Internal fixation of diaphyseal fractures of the forearm by interlocking intramedullary nail: short-term results in eighteen patients.

OBJECTIVE: This study was designed to evaluate the efficacy of the treatment of diaphyseal fractures of the forearm using the ForeSight forearm interlocking intramedullary nail. DESIGN: Retrospective study. SETTING: University-affiliated teaching hospital. PATIENTS: Eighteen patients with 32 displaced diaphyseal forearm fractures were identified. INTERVENTION: All fractures were treated with the ForeSight forearm interlocking intramedullary nail. Eighteen fractures were stabilized with static interlocking technique. MAIN OUTCOME MEASURES: The assessment of patients was based on the time to union, the functional recovery, and the incidence of complications. Physical capability was evaluated by using the rating system of Grace and Eversmann. Patient-rated outcome was assessed by completion of the Disability of Arm Shoulder Hand questionnaire (DASH). RESULTS: All fractures healed with the index procedure. The average time to union for fractures utilizing a closed technique was 10 weeks; for fractures using an open reduction technique, 15 weeks. The mean pronation was 62 (range, 0-96) degrees, and the mean supination was 80 (range, 0-105) degrees. Compared with the normal arm, the mean loss of rotation of the forearm was 32 (range, 5-162) degrees. Using the rating system of Grace and Eversmann, 13 patients had an excellent or good result, 3 had an acceptable result, and 2 had an unacceptable result. Using the patient-rated functional questionnaire, the mean DASH of 19 (range, 4-72) points at the time of the most recent follow-up indicated a mild-to-moderate impairment. There were 7 postoperative complications. The incidence of complications was 22% (7/32). One cross-union between forearm bones occurred in a patient with a closed head injury and high-energy trauma. Two nondriving end screws of the ulna nail backed out causing wrist pain and had to be removed. There were 4 superficial infections occurring all in the fractures that necessitated an open reduction technique. The overall rate of infection was 12.5% (4/32). Three patients who presented with an open fracture needed a skin graft to cover the open wound. CONCLUSIONS: Forearm interlocking intramedullary nailing is an acceptable method to stabilize displaced diaphyseal forearm fractures in adult.

Adult↗