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We assessed operatively treated closed distal radial fractures to identify independent risk factors for surgical site infection after treatment. A retrospective review was carried out of 531 operatively treated closed distal radial fractures over a 5-year period. Multiple logistic regression was performed with infection as the dependent variable, using a stepwise regression procedure to select variables to construct the final model. In total, 19 (3.6%) fractures were complicated by postoperative surgical site infection. Uncontrolled diabetes with HbA1c >7, the presence of external fixation or external Kirschner wires, and tobacco use were significant independent predictors of infection. Age and time in the operating room were also statistically significant predictors but deemed to be not clinically meaningful. Level of evidence: IV [ABSTRACT FROM AUTHOR]

Background: Pollicization of the index finger is a rarely performed reconstructive option for patients with total thumb amputations with nonsalvageable carpometacarpal (CMC) joint and thenar muscles. Successful pollicization can provide basic grasp and pinch to help patients carry out activities of daily living. We present a retrospective review of 4 patients who underwent index finger pollicization for traumatic total thumb amputations. Methods: A retrospective review of 4 cases of pollicization using an injured index finger for traumatic thumb amputation was performed. Patients available for follow-up were contacted for functional assessment. Outcomes including range of motion (ROM), grip strength, key pinch, 2-point discrimination, and Disabilities of the Arm, Shoulder, and Hand score were obtained. Functional thenar muscle and the CMC joint were absent in all cases. Injury mechanism was firework in 2 patients and crush in 2 patients. Results: The time from injury to pollicization ranged from 8 days to 17 months. Follow-up time ranged from 10 weeks to 3 years. Three patients regularly used the pollicized thumb in activities of daily living such as writing. Tip pinch and lateral pinch along with grip strength were weak in all cases; the best recorded pinch strength was 24% and grip strength was 25% compared with the contralateral hand. The ROM of the pollicized thumb was limited. Conclusions: Index finger pollicization following total thumb amputation can be a viable last-resort option for patients. The pollicized digit acts as a sensate post and avoids further morbidity from the traumatized extremity. [ABSTRACT FROM AUTHOR]

The present study was designed to determine the production of nicotinic acid adenine dinucleotide phosphate (NAADP) and its role associated with lysosomes in mediating endothelin-1 (ET-1)-induced vasoconstriction in coronary arteries. HPLC assay showed that NAADP was produced in coronary arterial smooth muscle cells (CASMCs) via endogenous ADP-ribosyl cyclase. Fluorescence microscopic analysis of intracellular [Ca.sup.2+] concentration ([[[Ca.sup.2+]].sub.i]) in CASMCs revealed that exogenous 100 nM NAADP increased [[[Ca.sup.2+]].sub.i] by 711 [+ or -] 47 nM. Lipid bilayer experiments, however, demonstrated that NAADP did not directly activate ryanodine (Rya) receptor [Ca.sup.2+] release channels on the sarcoplasmic reticulum. In CASMCs pretreated with 100 nM bafilomycin A1 (Bat), an inhibitor of lysosomal [Ca.sup.2+] release and vacuolar proton pump function, NAADP-induced [[[Ca.sup.2+]].sub.i] increase was significantly abolished. Moreover, ET-1 significantly increased NAADP formation in CASMCs and resulted in the rise of [[[Ca.sup.2+]].sub.i] in these cells with a large increase in global [Ca.sup.2+] level of 1,815 [+ or -] 84 nM. Interestingly, before this large [Ca.sup.2+] increase, a small [Ca.sup.2+] spike with an increase in [[[Ca.sup.2+]].sub.i] of 529 [+ or -] 32 nM was observed. In the presence of Baf (100 nM), this ET-1-induced two-phase [[[Ca.sup.2+]].sub.i] response was completely abolished, whereas Rya (50 [micro]M) only markedly blocked the ET-1-induced large global [Ca.sup.2+] increase. Functional studies showed that 100 nM Baf significantly attenuated ET-1-induced maximal constriction from 82.26 [+ or -] 4.42% to 51.80 [+ or -] 4.36%. Our results suggest that a lysosome-mediated [Ca.sup.2+] regulatory mechanism via NAADP contributes to ET-1-induced [Ca.sup.2+] mobilization in CASMCs and consequent vasoconstriction of coronary arteries. [beta]-nicotinamide adenine dinucleotide phosphate; adenosine 5'-diphosphate-ribosyl cyclase; coronary artery; vascular smooth muscle

The present study tested the hypothesis that cyclic ADP ribose (cADPR) serves as a novel second messenger to mediate intracellular [Ca.sup.2+] mobilization in coronary arterial endothelial cells (CAECs) and thereby contributes to endothelium-dependent vasodilation. In isolated and perfused small bovine coronary arteries, bradykinin (BK)-induced concentration-dependent vasodilation was significantly attenuated by 8-bromocADPR (a cell-permeable cADPR antagonist), ryanodine (an antagonist of ryanodine receptors), or nicotinamide (an ADP-ribosyl cyclase inhibitor). By in situ simultaneously fluorescent monitoring, [Ca.sup.2+] transient and nitric oxide (NO) levels in the intact coronary arterial endothelium preparation, 8-bromo-cADPR (30 [micro]M), ryanodine (50 [micro]M), and nicotinamide (6 mM) substantially attenuated BK (1 [micro]M)induced increase in intracellular [[Ca.sup.2+]] by 78%, 80%, and 74%, respectively, whereas these compounds significantly blocked BK-induced NO increase by about 80%, and inositol 1,4,5-trisphosphate receptor blockade with 2-aminethoxydiphenyl borate (50 [micro]M) only blunted BK-induced [Ca.sup.2+]-NO signaling by about 30%. With the use of cADPR-cycling assay, it was found that inhibition of ADP-ribosyl cyclase by nicotinamide substantially blocked BK-induced intracellular cADPR production. Furthermore, HPLC analysis showed that the conversion rate of [beta]-nicotinamide guanine dinucleotide into cyclic GDP ribose dramatically increased by stimulation with BK, which was blockable by nicotinamide. However, U-73122, a phospholipase C inhibitor, had no effect on this BK-induced increase in ADP-ribosyl cyclase activity for cADPR production. In conclusion, these results suggest that cADPR importantly contributes to BK- and A-23187-induced NO production and vasodilator response in coronary arteries through its [Ca.sup.2+] signaling mechanism in CAECs. nucleotide; vasodilation; endothelium; endothelium-derived relaxing factor

The present study tested the hypothesis that endostatin stimulates superoxide ([O.sup.-.sub.2]*) production through a ceramide-mediating signaling pathway and thereby results in an uncoupling of bradykinin (BK)-induced increases in intracellular [Ca.sup.2+] concentration ([[[Ca.sup.2+]].sub.i]) from nitric oxide (NO) production in coronary endothelial cells. With the use of high-speed, wavelength-switching, fluorescence-imaging techniques, the [[[Ca.sup.2+]].sub.i] and NO levels were simultaneously monitored in the intact endothelium of freshly isolated bovine coronary arteries. Under control conditions, BK was found to increase NO production and [[[Ca.sup.2+]].sub.i] in parallel. When the arteries were pretreated with 100 nM human recombinant endostatin for 1 h, this BK-induced NO production was reduced by 89%, whereas [[[Ca.sup.2+]].sub.i] was unchanged. With the conversion rate of L-[[sup.3.H]]arginine to L-[[sup.3.H]citrulline measured, endostatin had no effect on endothelial NO synthase (NOS) activity, but it stimulated ceramide by activation of sphingomyelinase (SMase), whereby [O.sup.-.sub.2]* production was enhanced in endothelial cells. [O.sup.-.sub.2]*. scavenging by tiron and inhibition of NAD(P)H oxidase by apocynin markedly reversed the effect of endostatin on the NO response to BK. These results indicate that endostatin increases intracellular ceramide levels, which enhances [O.sup.-.sub.2]* production through activation of NAD(P)H oxidase. This ceramide-[O.sup.-.sub.2]* signaling pathway may contribute importantly to endostatin-induced endothelial dysfunction. collagen; sphingolipid; free radicals; signal transduction; coronary artery

Recent studies have indicated that urotensin II (UII), a cyclic peptide, is vasoactive and may be involved in cardiovascular dysfunctions. It remains unknown, however, whether UII plays a role in the control of renal vascular tone and tubular function. In the present study, a continuous infusion of synthetic human UII (hUII) into the renal artery (RA) in anesthetized rats was found to increase renal blood flow (RBF) and urinary water and sodium excretion (UV and [U.sub.Na.]V) in a dose-dependent manner. At a dose of 20 ng*[kg.sup.-1]. [min.sup.-1], it increased RBF by 20% and UV and [U.sub.Na]V by 94 and 109%, respectively. Nitric oxide (NO) synthase inhibitor [N.sup.G]-nitro-L-arginine methyl ester (L-NAME) completely abolished hUII-induced increases in RBF and water/sodium excretion. In isolated, pressurized, and phenylephrine-precontracted small RA with internal diameter of ~200 [micro]m, hUII produced a concentration-dependent vasodilation with a maximal response of 55% at 1.5 [micro]M. L-NAME significantly blocked this hUII-induced vasodilation by 60%. In denuded RA, hUII had neither vasodilator nor vasoconstrictor effect. With the use of 4,5-diaminofluorescein diacetate-based fluorescence imaging analysis of NO levels, hUII (1 [micro]M) was shown to double the NO levels within the endothelium of freshly dissected small RA, and L-NAME blocked this UII-induced production of endothelial NO. These results indicate that UII produces vasodilator and natriuretic effects in the kidney and that UII-induced vasodilation is associated with increased endothelial NO in the RA. natriuretic factor; renal circulation; sodium reabsorption; renal tubule; renal hemodynamics

The present study hypothesized that superoxide ([O.sup.-.sub.2]*) importantly contributes to the regulation of hypoxia-inducible factor (HIF)-1[alpha] expression at posttranscriptional levels in renal medullary interstitial cells (RMICs) of rats. By Western blot analysis, it was found that incubation of RMICs with [O.sup.-.sub.2]* generators xanthine/xanthine oxidase and menadione significantly inhibited the hypoxia- or [CoCl.sub.2]-induced increase in HIF-1[alpha] levels and completely blocked the increase in HIF-1[alpha] levels induced by ubiquitin-proteasome inhibition with CBZ-LLL in the nuclear extracts from these cells. Under normoxic conditions, a cell-permeable [O.sup.-.sub.2]* dismutase (SOD) mimetic, 4-hydroxyl-tetramethylpiperidin-oxyl (TEMPOL) and PEG-SOD, significantly increased HIF-1[alpha] levels in RMICs. Two mechanistically different inhibitors of NAD(P)H oxidase, diphenyleneiodonium and apocynin, were also found to increase HIF-1[alpha] levels in these renal cells. Moreover, introduction of an anti-sense oligodeoxynucleotide specific to NAD(P)H oxidase subunit, [p22.sup.phox], into RMICs markedly increased HIF-1[alpha] levels. In contrast, the OH. scavenger tetramethylthiourea had no effect on the accumulation of HIF-1[alpha] in these renal cells. By Northern blot analysis, scavenging or dismutation of [O.sup.-.sub.2]* by TEMPOL and PEG-SOD was found to increase the mRNA levels of an HIF-1[alpha]-targeted gene, heme oxygenase-1. These results indicate that increased intracellular [O.sup.-.sub.2] levels induce HIF-1[alpha] degradation independently of [H.sub.2][O.sub.2] and OH* radicals in RMICs. NAD(P)H oxidase activity may importantly contribute to this posttranscriptional regulation of HIF-1[alpha]* in these cells under physiological conditions. reactive oxygen species; gene transcription; anoxia; renal interstitium; renal medulla

Background: Skeletal muscle lacerations are a relatively common injury. Compared with nonrepaired lacerations, surgically repaired muscle lacerations regenerate faster, develop less scar tissue, have a higher return to baseline strength, and have lower incidence of hematomas. Despite the benefits of repair, the optimal repair technique is still unknown. The purpose of this study was to examine the biomechanical properties of common muscle repair techniques to determine the optimal repair. Methods: Forty-two fusiform porcine muscle specimens were dissected and used for this study. Three suture techniques were used for comparative analysis: Figure-eight, Mason Allen, and Perimeter. Each muscle was transected and then repaired using one of the 3 techniques. Fourteen muscle-tendon specimens were prepared for each group and tested for tensile failure using a material testing system. Biomechanical properties, including peak failure point and stiffness, were compared for differences between the suture groups by 1-way analysis of variance. The average time per repair technique was also recorded. Results: The Perimeter technique showed a statistically significant higher peak failure point than the Mason Allen technique (P =.03). Both the Figure-eight (P =.047) and Perimeter techniques (P <.001) were significantly stiffer than the Mason Allen technique. The repair time was comparable across all 3 techniques. Conclusions: The Figure-eight and Perimeter repairs were found to be similar in peak failure point and stiffness, whereas the Mason Allen technique showed significantly lower stiffness and peak failure point. The Figure-eight was the quickest repair to perform. The Figure-eight technique may be strongly considered for muscle laceration repairs due to its simplicity and efficiency. [ABSTRACT FROM AUTHOR]

The advent of three-dimensional (3D) printing in the 1980s ushered in a new era of manufacturing. Original 3D printers were large, expensive and difficult to operate, but recent advances in 3D printer technologies have drastically increased the accessibility of these machines such that individual surgical departments can now afford their own 3D printers. As adoption of 3D printing technology has increased within the medical industry so too has the number of 3D printable materials. Selection of the appropriate printer and material for a given application can be a daunting task for any clinician. This review seeks to describe the benefits and drawbacks of different 3D printing technologies and the materials used therein. Commercially available printers using fused deposition modelling or fused filament fabrication technology and relatively inexpensive thermoplastic materials have enabled rapid manufacture of anatomic models and intraoperative tools as well as implant prototyping. Titanium alloys remain the gold-standard material for various implants used in the fixation of craniofacial or extremity fractures, but polymers and ceramics are showing increasing promise for these types of applications. An understanding of these materials and their compatibility with various 3D printers is essential for application of this technology in a healthcare setting. [ABSTRACT FROM AUTHOR]