Prospective evaluation of sleep improvement after cubital tunnel decompression surgery.

BACKGROUND: Compromised sleep is a known phenomenon with compressive neuropathies such as carpal tunnel syndrome. However, the prevalence of sleep disturbance with cubital tunnel syndrome (CuTS) and the effect on sleep after ulnar nerve decompression are not well understood. We hypothesized that CuTS results in sleep disturbances and that decompression surgery would result in improvement in overall sleep quality. METHODS: Consecutive patients with electrodiagnostic-proven CuTS indicated for decompression were prospectively enrolled. Demographic data, McGowan grade, electrodiagnostic (electromyography) severity, visual analog scale pain score, the 11-item version of the Disabilities of the Arm, Shoulder and Hand questionnaire, and the Insomnia Severity Index scale data were collected preoperatively and at 2 weeks and 3 months postoperatively. RESULTS: There were 145 patients enrolled, with 97% available at 2 weeks and 72% available at the final 3-month follow-up. Surgical decompression procedures consisted of 102 in situ releases and 43 transpositions. The average preoperative Insomnia Severity Index score for the entire cohort was 10.7, above the threshold for a diagnosis of insomnia, which subsequently improved to 4.1 by final follow-up postoperatively, consistent with resolution of the insomnia. There was no difference in the extent of sleep improvement between in situ decompression and transposition. Similarly, electromyography severity and McGowan grade also did not appear to significantly affect the extent of sleep improvement. CONCLUSION: CuTS decompression surgery, irrespective of surgical type and preoperative severity, resulted in improvement in sleep by the 3 month postoperative visit.

Thumb-Basal Joint Arthroplasty Outcomes and Metacarpal Subsidence: A Prospective Cohort Analysis of Trapeziectomy With Suture Button Suspensionplasty Versus Ligament Reconstruction With Tendon Interposition.

BACKGROUND: Thumb carpometacarpal (CMC) joint arthroplasty is a common procedure in the surgical management of symptomatic thumb basal joint arthritis. Following trapeziectomy, a number of suspensionplasty techniques are often used, but limited comparative evidence exists between these techniques. The central aim of this study was to prospectively compare the outcomes of 2 suspensionplasty techniques following trapeziectomy: suture button (TightRope) versus ligament reconstruction and tendon interposition (LRTI). METHODS: Prospective data were collected on 112 consecutive patients with Eaton stage III-IV thumb CMC arthritis who underwent open trapeziectomy and suspensionplasty. There were 53 LRTI and 59 TightRope suspensionplasty procedures. Outcomes were measured using the Quick Disabilities of the Arm, Shoulder, and Hand (QuickDASH) questionnaire, Visual Analogue Scale (VAS) for pain, radiographic analysis, and lateral pinch strength. Patient demographic data and complications were also recorded. RESULTS: Patients undergoing TightRope suspensionplasty had significantly higher trapeziometacarpal index and thus less subsidence than the LRTI group at 2 weeks (0.22 vs 0.17 [P < .0001]) and 3 months (0.17 vs 0.15 [P < .05]) postoperatively. TightRope suspensionplasty also had a significantly lower QuickDASH score at 2 weeks (64.7 vs 74.6 [P < .05]), 3 months (20.7 vs 32.5 [P < .05]), and 1 year postoperatively (7.57 vs 21.5 [P < .05]) compared with the LRTI group. However, there was no difference in VAS pain, lateral pinch strength, reoperation, or complications at any time point between groups. CONCLUSIONS: Thumb CMC joint arthroplasty performed with a TightRope suspensionplasty versus LRTI yielded short-term improved resistance to subsidence, long-term greater improvement in clinical outcome by QuickDASH, and no difference in pain or complication rates.

Biliverdin protects against the deterioration of glucose tolerance in db/db mice.

AIMS/HYPOTHESIS: We have previously shown a negative correlation between serum bilirubin levels and prevalence of type 2 diabetes, suggesting that bilirubin inhibits development of this disease. To confirm this hypothesis, we investigated whether administration of biliverdin, the precursor of bilirubin, protects against the deterioration of glucose tolerance in db/db mice, a rodent model of type 2 diabetes. METHODS: Biliverdin (20 mg/kg daily) was orally administered to 5-week-old db/db mice for 4 weeks. After 4 weeks of treatment, i.p. glucose tolerance and insulin tolerance tests were performed. Insulin content was evaluated by immunostaining and ELISA. Oxidative stress markers (8-hydroxy-2'-deoxyguansosine and dihydroethidium staining) and expression of NADPH oxidase components Pdx1 and Bax were also evaluated in isolated islets. RESULTS: Treatment with biliverdin partially prevented worsening of hyperglycaemia and glucose intolerance in db/db mice. This effect was accompanied by a significant increase in insulin content and Pdx1 expression, and a significant decrease of apoptosis and Bax expression in pancreatic islets from db/db mice. At the same time, levels of oxidative stress markers and NADPH oxidase component production in islets were normalised. Biliverdin had little effect on HOMA of insulin resistance or insulin resistance evaluated by insulin tolerance tests. CONCLUSIONS/INTERPRETATION: Biliverdin may protect against progressive worsening of glucose tolerance in db/db mice, mainly via inhibition of oxidative stress-induced beta cell damage.

Adsorption behaviors of poly(N-p-vinylbenzyl-4-o-beta-d-galactopyranosyl-[1-->4]-d-gluconamide) by quartz-crystal microbalance.

Adsorption behaviors of amphiphilic poly(N-p-vinylbenzyl-4-o-beta-d-galactopyranosyl-[1-->4]-d-gluconamide) (PVLA) on the polystyrene (PS) surface was studied using 27 MHz quartz-crystal microbalance (QCM). The amount of adsorbed PVLA on PS surface was increased with an increase of PVLA concentration as a Langmuir-type in a monolayer. The saturated mass change (DeltaM(max)) and association constant (K(a)) of PVLA on PS surface were 498.6 ng/cm(2) and 1.93 x 10(7)M(-1), respectively. The adsorbed PVLA on PS surface was specifically recognized by Allo A lectin due to specific interaction between galactose moieties in the PVLA and Allo A. The hydrophobic interaction between hydrophobic main chain of PVLA and hydrophobic surface of PS was reduced in the presence of urea and the diameter of PVLA aqueous solution was decreased with an increase of urea concentration.

Inhibition of HIV-1 Nef-induced apoptosis of uninfected human blood cells by serine/threonine protein kinase inhibitors, fasudil hydrochloride and M3.

The Nef protein of HIV-1 binds to and induces apoptotic cytolysis of uninfected but activated human peripheral blood mononuclear cells (PBMC) and various cell line cells derived from CD4+ T, CD8+ T and B lymphocytes, macrophages, and neutrophils. The Nef-induced apoptosis also occurs with blood cells not expressing CD95 (Fas). The Nef-induced apoptosis as well as Fas-mediated apoptosis was inhibited by acetyl-Try-Val-Ala-Asp-CHO, an IL-1beta converting enzyme (ICE) inhibitor. On the other hand, serine/threonine protein kinase (PK) inhibitors, H-7, fasudil hydrochloride and M3, inhibited the Nef-induced apoptosis, and not the Fas-mediated one, without affecting the cell-binding activity of Nef and Nef-binding capacity of the activated cells. Preincubation of the cells with the drugs before being bound by Nef was required for the inhibition of apoptosis. These results suggest that the PK inhibitors specifically act on a cellular protein involved in the upper stream of signal transduction pathway of the Nef-induced apoptosis, which is different from the Fas-mediated pathway but meets it upstream of ICE. In addition, the drugs suppressed the cellular activation-associated cell surface expression of a putative Nef-binding protein in PBMC, although they had no influence on its expression in cell line cells. These findings suggest the feasibility of clinical use of the PK inhibitors to prevent the development of AIDS by inhibiting the Nef-induced apoptosis of uninfected blood cells.

Nef protein of HIV-1 induces apoptotic cytolysis of murine lymphoid cells independently of CD95 (Fas) and its suppression by serine/threonine protein kinase inhibitors.

The Nef protein of HIV-1 is suggested to play a role in depletion of uninfected CD4+ T cells leading to the development of AIDS. The recombinant soluble Nef protein was shown to bind to cell surfaces of various murine lymphoid cell lines, including T and B lymphocytes, mastocytoma cells and macrophages. Cross-linking of the cell-bound Nef protein with anti-Nef antibodies induced apoptotic cytolysis of the cells. Although primary lymphocytes from young mice resisted Nef binding and Nef-induced cytolysis, treatment of the cells with concanavalin A or phytohemagglutinin made them susceptible to these activities, indicating that cellular activation is required for the apoptosis. The Nef-induced apoptosis also occurred with murine cells not expressing CD95 (Fas). These findings were quite similar to those obtained for human blood cells, suggesting that the mouse is applicable for analysis of Nef activities. The Nef-induced apoptosis was efficiently suppressed by serine/threonine protein kinase inhibitors, H7, fasudil hydrochloride and M3, which did not inhibit CD95 (Fas)-mediated apoptosis. On the other hand, bisindolylmaleimide, a protein kinase C inhibitor which inhibits CD95 (Fas)-mediated apoptosis, did not affect Nef-induced apoptosis. These results suggest that the Nef-induced apoptosis of murine cells involved a serine/threonine protein kinase-dependent signal transduction pathway distinct from the CD95 (Fas)-mediated system.

HIV-1 Nef protein-induced apoptotic cytolysis of a broad spectrum of uninfected human blood cells independently of CD95(Fas).

The Nef protein of HIV-1 binds to uninfected CD4+T lymphocytes and induces apoptotic cytolysis of the cells. We examined several human blood cell lines and peripheral blood mononuclear cells (PBMCs) for Nef-induced apoptotic cell death. Soluble Nef protein was shown to bind to the cell surface of not only CD4+T cells but also CD8+T lymphocytes, B lymphocytes, macrophages and neutrophils. PBMCs from normal subjects resisted Nef binding, and activation of the cells with phytohemagglutinin or concanavalin A converted the cells to be susceptible to the binding. Cross-linking of the Nef proteins bound to the cell surfaces with anti-Nef antibody-induced apoptotic cytolysis of the cells. The Nef-mediated apoptosis occurred independently of CD95(Fas). These results suggest that soluble Nef protein, which is found in sera of HIV-1 infected patients, is involved in the destruction of a broad spectrum of uninfected blood cells leading to immune suppression.

Effects of recombinant human soluble thrombomodulin (rhs-TM) on a rat model of disseminated intravascular coagulation with decreased levels of plasma antithrombin III.

We reported that recombinant human soluble thrombomodulin (rhs-TM) is effective for disseminated intravascular coagulation (DIC) in vivo, in mice and rats. In the present work, we investigated the effects of decreased plasma antithrombin III (ATIII) levels on anticoagulant effects of rhs-TM, as compared to findings with heparin, of which effect is lowered by the decreased plasma ATIII levels in patients with DIC. Rat plasma ATIII levels decreased when we mixed plasma with anti-rat ATIII antibody and the potential of heparin to prolong APTT or PT was markedly diminished. The potential of rhs-TM to prolong APTT and PT was not affected. In rats injected with anti-rat ATIII antibody, plasma ATIII levels decreased immediately. When the rats were infused with tissue factor (TF), DIC was induced. At doses of rhs-TM and heparin which were equally effective at inhibiting the decrease in platelet count and fibrinogen level in control rats treated with TF, only rhs-TM remained effective in preventing DIC in rats with reduced ATIII levels. Heparin was not effective when administered to these rats with reduced ATIII levels. Therefore, rhs-TM effectively inhibits coagulation independent of ATIII levels, in contrast to heparin, which depends on the ATIII level.

Receptor-mediated cell modulator delivery to hepatocyte using nanoparticles coated with carbohydrate-carrying polymers.

Cell modulators such as colchicine (CO), cytochalasin B (CY) and taxol (TX) loaded nanoparticles coated with carbohydrate-carrying polymers, as hepatocyte-specific targeting material using galactose ligands as recognition signals to asialoglycoprotein receptors were prepared by the diafiltration method. Effects of cell modulators from their loaded nanoparticles on morphology of hepatocytes were studied. Receptor-mediated endocytosis of the nanoparticles were examined by fluorescence and confocal laser microscopy. It was found that the shapes of most hepatocytes were changed for the CY-loaded, TX-loaded, or CO-loaded nanoparticles whereas their shapes were not changed in comparison with control when CY, TX, or CO were mixed with the nanoparticles. From the fluorescence and confocal laser microscopic studies, it is suggested that the nanoparticles coated with sugar-carrying polymers were internalized by the hepatocytes through the receptor-mediated mechanism.

Simple preparation of nanoparticles coated with carbohydrate-carrying polymers.

Nanoparticles bearing carbohydrate chains on the surface can be prepared by the simple diafiltration method. The nanoparticles prepared by the present method displayed high yield, no-aggregation formation, small size, narrow size distribution, and one-step procedure. Also, the high density carbohydrate chains on the particles can be recognized by liver cells.

Specific interaction between erythrocytes and a glucose-carrying polymer mediated by the type-1 glucose transporter (GLUT-1) on the cell membrane.

A reducing glucose-carrying polymer, called poly [3-O-(4'-vinylbenzyl)-D-glucose] (PVG), interacted with erythrocytes carrying the type-1 glucose transporter (GLUT-1) on the cell membrane. The cooperative interaction between a number of GLUT-1s and a number of reducing 3-O-methyl-D-glucose moieties on a PVG polymer chain is responsible for the increase in the interaction with erythrocytes. In contrast to the PVG homopolymer, other sugar-carrying polymers showed lower interaction with erythrocytes. The affinity of erythrocytes and PVG was studied using FITC-labeled glycopolymers. The fluorescence intensity significantly changed, whereas a small change in fluorescence intensity was observed for other homopolymers. The specific interaction between GLUT-1 on erythrocytes and the PVG polymer carrying reducing glucose was suppressed by the inhibitors, phloretin, phloridzin, and cytochalasin B, and a monoclonal antibody to GLUT-1. Direct observation by confocal laser microscopy with the use of FITC-labeled PVG demonstrated that erythrocytes interacted with the soluble form of the PVG polymer via GLUT-1, while fluorescence labeling of the cell surface was prevented on pretreatment with the monoclonal antibody to GLUT-1.

Central cystadenocarcinoma of the mandible.

Papillary cystadenocarcinoma (PCAC) of the salivary gland is a rare malignant tumour and occurs in major and minor salivary glands. PCAC of the mandible is exceptionally rare; only 2 cases have been reported. In this study, the authors report a case of PCAC within the mandible. The patient presented with a painful right mandibular mass that had gradually increased in size. The lesion appeared radiographically as a well-demarcated multilocular radiolucent area, similar to an odontogenic cystic lesion. The authors present a case of PCAC with reference to the relevant literature.

Lens exposure during brain scans using multidetector row CT scanners: methods for estimation of lens dose.

BACKGROUND AND PURPOSE: Some recent studies on radiation lens injuries have indicated much lower dose thresholds than specified by the current radiation protection guidelines. The purpose of this research was to measure the lens dose during brain CT scans with multidetector row CT and to assess methods for estimating the lens dose. MATERIALS AND METHODS: With 8 types of multidetector row CT scanners, both axial and helical scans were obtained for the head part of a human-shaped phantom by using normal clinical settings with the orbitomeatal line as the baseline. We measured the doses on both eyelids by using an RPLGD during whole-brain scans including the orbit with the starting point at the level of the inferior orbital rim. To assess the effect of the starting points on the lens doses, we measured the lens doses by using 2 other starting points for scanning (the orbitomeatal line and the superior orbital rim). RESULTS: The CTDIvols and the lens doses during whole-brain CT including the orbit were 50.9-113.3 mGy and 42.6-103.5 mGy, respectively. The ratios of lens dose to CTDIvol were 80.6%-103.4%. The lens doses decreased as the starting points were set more superiorly. The lens doses during scans from the superior orbital rim were 11.8%-20.9% of the doses during the scans from the inferior orbital rim. CONCLUSIONS: CTDIvol can be used to estimate the lens dose during whole-brain CT when the orbit is included in the scanning range.

Role of E-cadherin molecules in spheroid formation of hepatocytes adhered on galactose-carrying polymer as an artificial asialoglycoprotein model.

The role of E-cadherin in the spheroid formation of hepatocytes adhered on the poly(N-p-vinylbenzyl-D-lactonamide) (PVLA) as a model ligand for asialoglycoprotein receptors (ASGP-R) of hepatocytes was studied. Expression of E-cadherin was increased in round hepatocytes adhered on a high-coating density of PVLA (100 microg/ml), and also in flat ones adhered on a low-coating density of PVLA (1 microg/ml) in the presence of epidermal growth factor (EGF). Hepatocyte spheroids formed on the high-coating density of PVLA in the presence of EGF after 48 h were inhibited by an anti-E-cadherin monoclonal antibody (ECCD-1). From immunofluorescence and confocal laser microscopy, E-cadherin was localized in the intercellular boundaries and concentrated at the inside surface of aggregated cells. As a result, E-cadherin could play an important role in hepatocyte assembly.

Naftopidil, a novel alpha1-adrenoceptor antagonist, displays selective inhibition of canine prostatic pressure and high affinity binding to cloned human alpha1-adrenoceptors.

The pharmacological profiles of the alpha1-adrenoceptor antagonists naftopidil, tamsulosin and prazosin were studied in an anesthetized dog model that allowed the simultaneous assessment of their antagonist potency against phenylephrine-mediated increases in prostatic pressure and mean blood pressure. The intravenous administration of each of these compounds dose-dependently inhibited phenylephrine-induced increases in prostatic pressure and mean blood pressure. To further assess the ability of the three compounds to inhibit phenylephrine-induced responses, the doses required to produce a 50% inhibition of the phenylephrine-induced increases in prostatic and mean blood pressure and the selectivity index obtained from the ratio of those two doses were determined for each test compound. Forty minutes after the intravenous administration of naftopidil, the selectivity index was 3.76, and those of tamsulosin and prazosin were 1.23 and 0.61, respectively. These findings demonstrated that naftopidil selectively inhibited the phenylephrine-induced increase in prostatic pressure compared with mean blood pressure in the anesthetized dog model. The selectivity of naftopidil for prostatic pressure was the most potent among the test compounds. In addition, using cloned human alpha1-adrenoceptor subtypes, naftopidil was selective for the alpha1d-adrenoceptor with approximately 3- and 17-fold higher affinity than for the alpha1a- and alpha1b-adrenoceptor subtypes, respectively. The selectivity of naftopidil for prostatic pressure may be attributable to its high binding affinity for alpha1a- and alpha1d-adrenoceptor subtypes.

Effects of atrial natriuretic peptide on ischemic brain edema in rats evaluated by proton magnetic resonance method.

We examined the effect of atrial natriuretic peptide on cerebral edema in 96 rats. Forty-four rats were given 30 (n = 11), 120 (n = 26), or 150 (n = 7) micrograms/kg of the peptide intravenously over 24 hours after occlusion of the left middle cerebral artery to induce cerebral ischemia. We then measured the brain water content, the brain sodium and potassium contents, the in vitro proton nuclear magnetic resonance longitudinal (T1) and transverse (T2) relaxation times, and the area of the edematous regions. Compared with saline treatment (n = 39), peptide treatment decreased the brain water content in a dose-dependent manner and decreased the brain sodium content significantly (p less than 0.05). Peptide treatment also suppressed the lengthening of both T1 and T2 in edematous tissue (p less than 0.05 and p less than 0.01, respectively) and reduced the area of the edematous regions observed by magnetic resonance imaging (p less than 0.01). Atrial natriuretic peptide appears to have a pharmacological effect on ischemic brain edema, possibly by suppressing the elevation of water content through regulation of electrolyte transport in the brain.

[Experimental study of flow rates in microcatheters using various kinds of contrast materials: comparison of imaging capability by iodine delivery rates].

In order to establish the optimal injection technique for abdominal digital subtraction angiography (DSA), flow rate measurement was performed under various combinations of all the currently available iodinated contrast materials with two types of coaxial microcatheters. In vitro study was done utilizing a plastic model of the abdominal aorta with the tip of the catheter positioned at the presumed proper hepatic artery. A total of 20ml of contrast material was injected by a pressure injector at a rate of 3 ml/sec at 300 or 600 psi, and actual flow volume was measured. Imaging capability was evaluated by calculating iodine delivery rates (IDRs). IDRs were highest in iopamidol 300 mgI/ml and iomeperol 300 mgI/ml, nonionic monomeric contrast materials of medium concentration. The results suggest that the best quality DSA images with injection to the proper hepatic artery using a coaxial microcatheter can be obtained with nonionic monomeric contrast materials of medium concentration.

Patellofemoral complications following total knee arthroplasty. Correlation with implant design and patient risk factors.

Results of 211 total knee arthroplasty operations were retrospectively evaluated to identify patients with knees at greatest risk for the development of patellofemoral complications and to determine the incidence and type of patellofemoral complications associated with different patellar implants. Patellofemoral complications occurred in 27 knees (12.8%). Osteoarthritis and obesity were associated with an increased incidence of patellofemoral problems. Significantly higher rates of patellofemoral complications were noted with metal-backed patellar implants and with patellar components implanted without cement. The loosening rate with cementless fixation was 13.5%. The lowest rate of patellofemoral complications following total knee arthroplasty was obtained with all-polyethylene domed patellar components implanted with cement.

First presentation of polymyositis postpartum following intrauterine fetal death.

We present a case of polymyositis (PM) following intrauterine fetal death. The first presentation of PM in the patient was during postpartum. The patient was referred to our hospital because of a fever of unknown cause 13 d after delivery of dead fetus at 32 weeks' gestation. PM was diagnosed based on the increased serum creatine phosphokinase level, typical electromyogram findings and characteristic muscle biopsy findings.