Restorative Rehabilitation of the Cleft Affected Occlusion - A Service Evaluation.

Cleft Lip and/or Palate (CLP) is the most common cranio-facial abnormality thought to be caused by a combination of genetic and environmental factors causing challenges with feeding, dental development and speech. Cleft affected individuals often present a unique set of challenges with regards to their oro-facial and dental development and require multidisciplinary care. This article aims to describe the role of the restorative dentist in the multidisciplinary management of cleft affected individuals and outlines the various clinical presentations and restorative challenges. This article describes the various treatment modalities provided for cleft affected individuals under the National Health Service (NHS) at Liverpool University Dental Hospital (LUDH) and ranges from minimally invasive techniques to conventional fixed and removable prosthodontics.

State of the Art Management of Aortic Valve Disease in Ankylosing Spondylitis.

PURPOSE OF REVIEW: Cardiac involvement in patients with ankylosing spondylitis (AS) generally manifests itself as aortic insufficiency, aortitis, disturbance in cardiac conduction, and myocardial dysfunction. We have used a case-based approach to review the current state of the art knowledge regarding the diagnosis and management of aortic valve disease and aortitis in patients with AS. RECENT FINDINGS: The risk for aortic valve disease and aortic valve replacement or repair is significantly higher than in people without AS, and this risk increases with age. Echocardiography, cardiac MRI, and CT can serve as effective tools for screening and follow-up. Surgical repair/replacement remains the mainstay of therapy for aortic insufficiency and aortic dilation, whereas transcatheter-based techniques may be favorable in the setting of aortic stenosis. Aortic valve and atrioventricular conduction abnormalities contribute to overall cardiovascular burden in AS. Optimal timing and therapeutic technique are dependent on assessment of overall risk and serial follow-up.

Outbreaks of influenza-like illness in care homes in the East of England: impact of variations in neuraminidase inhibitor provision.

OBJECTIVES: To examine the differences in outcomes related to variable provision of antivirals in care home respiratory outbreaks. STUDY DESIGN: This is a retrospective observational study. METHODS: Routinely collected outbreak surveillance data reported from care home staff was recorded using a standard template and extracted from the Public Health England health protection electronic records. Data included numbers of people affected, provision of oseltamivir, hospitalization, and deaths during the outbreak in the care home. Oseltamivir provision was categorized by proportion of eligible residents prescribed it on advice. Additional data on microbiological diagnoses were obtained directly from the hospital laboratories. Logistic regression was used to examine associations between oseltamivir provision and hospitalizations and deaths in care homes. RESULTS: One hundred and sixty-eight outbreaks were reported from 28th July 2016 until 27th March 2017, affecting 1459 residents and 347 staff. There were 76 hospital admissions and 37 deaths overall. Although deaths and hospital admissions also occurred in outbreaks caused by other respiratory viruses, outbreaks caused by influenza had the highest median number of people affected and a greater proportion of hospital admissions and deaths. Of the 56 outbreaks caused by influenza, there was a significant increase in the odds of the care home reporting deaths when oseltamivir was not used (odds ratio = 8.15, 95% confidence interval = 1.38-48.20, P = 0.02). There were also non-significant reductions in duration of outbreak and hospital admissions in care home outbreaks with oseltamivir treatment. CONCLUSIONS: Partial or no provision of oseltamivir was associated with poorer outcomes in laboratory-confirmed influenza outbreaks.

Toxigenic Corynebacterium ulcerans infection in a veterinary student in London, United Kingdom, May 2010.

We report on a case of toxigenic Corynebacterium ulcerans infection in a fully immunised veterinary student, investigated in London, United Kingdom, in May 2010. There was no ongoing transmission in human contacts. Possible animal sources were identified.

Tumor necrosis factor-alpha gene and protein expression in adult feline myocardium after endotoxin administration.

TNF alpha mRNA and protein biosynthesis were examined in the adult feline heart after stimulation with endotoxin. When freshly isolated hearts were stimulated with endotoxin in vitro, de novo TNF alpha mRNA expression occurred within 30 min, and TNF alpha protein production was detected within 60-75 min; however, TNF alpha mRNA and protein production were not detected in diluent-treated hearts. Immunohistochemical studies localized TNF alpha to endothelial cells, smooth muscle cells, and cardiac myocytes in the endotoxin-treated hearts, whereas TNF alpha immunostaining was absent in the diluent-treated hearts. To determine whether the cardiac myocyte was a source for TNF alpha production, two studies were performed. First, in situ hybridization studies, using highly specific biotinylated probes, demonstrated TNF alpha mRNA in cardiac myocytes from endotoxin-stimulated hearts; in contrast, TNF alpha mRNA was not expressed in myocytes from diluent-treated hearts. Second, TNF alpha protein production was observed when cultured cardiac myocytes were stimulated with endotoxin, whereas TNF alpha protein production was not detected in the diluent-treated cells. The functional significance of the intramyocardial production of TNF alpha was determined by examining cell motion in isolated cardiac myocytes treated with superfusates from endotoxin- and diluent-stimulated hearts. These studies showed that cell motion was depressed in myocytes treated with superfusates from the endotoxin-treated hearts, but was normal with the superfusates from the diluent-treated hearts; moreover, the negative inotropic effects of the superfusates from the endotoxin-treated hearts could be abrogated completely by pretreatment with an anti-TNF alpha antibody. Finally, endotoxin stimulation was also shown to result in the intramyocardial production of TNF alpha mRNA and protein in vivo. Thus, this study shows for the first time that the adult mammalian myocardium synthesizes biologically active TNF alpha.

Advances in the percutaneous treatment of aortic and mitral valve disease.

The healthcare burden of valvular heart disease continues to increase as our population ages. Because of advances in operative techniques and cardiac anesthesiology, surgery has excellent safety and durability for many patients, and surgery remains the gold standard for treating valvular heart disease. Because many patients have comorbidities that increase operative risk, interest in catheter-based valve repair and replacement has grown. Early human experience with aortic stent-valve prostheses has been quite encouraging. For mitral regurgitation, percutaneous annuloplasty and leaflet repair are being developed by numerous companies, and early human studies have demonstrated feasibility of percutaneous repair. Continuing advances in technology and experience promise to expand the role of percutaneous repair and replacement in the treatment of valvular heart disease. Ongoing trials will help define long-term durability and safety, along with appropriate patient selection for percutaneous treatment.

Assessment of total thrombus load in symptomatic patients with venous thromboembolism.

Pulmonary embolism (PE) and Deep vein thrombosis (DVT) are separate but related aspects of the same dynamic process termed as venous thrombembolism (VTE). The existing Asian literature has shown a wide variation in the prevalence of VTE, with very limited data from the Indian subcontinent. Between January 2001 and July 2004, 1,552 patients with clinically suspected lower limb DVT underwent a combined ascending radionuclide venogram and lung perfusion scan for assessment of the total thrombus burden. Of 744 patients with radionuclide venography proven DVT, 294 (40%) had a high probability lung scan. Nearly half of these patients were asymptomatic for pulmonary embolism. The high prevalence of PE in patients with DVT suggests the need for evaluation of thrombus load in the venous as well as pulmonary circulation. A combination radionuclide ascending venography with lung perfusion scan is a useful and reliable single test for this purpose.

Extent and direction of arterial remodeling in stable versus unstable coronary syndromes : an intravascular ultrasound study.

BACKGROUND: The morphological characteristics of coronary plaques in patients with stable versus unstable coronary syndromes have been described in vivo with intravascular ultrasound, but the relationship between arterial remodeling and clinical presentation is not well known. METHODS AND RESULTS: We studied 85 patients with unstable and 46 patients with stable coronary syndromes using intravascular ultrasound before coronary intervention. The lesion site and a proximal reference site were analyzed. The remodeling ratio (RR) was defined as the ratio of the external elastic membrane (EEM) area at the lesion to that at the proximal reference site. Positive remodeling was defined as an RR >1.05 and negative remodeling as an RR <0.95. Plaque area (13.9+/-5.5 versus 11.1+/-4.8 mm(2); P=0.005), EEM area (16.1+/-6.2 versus 13.0+/-4.8 mm(2); P=0. 004), and the RR (1.06+/-0.2 versus 0.94+/-0.2; P=0.008) were significantly greater at target lesions in patients with unstable syndromes than in patients with stable syndromes. Positive remodeling was more frequent in unstable than in stable lesions (51. 8% versus 19.6%), whereas negative remodeling was more frequent in stable lesions (56.5% versus 31.8%) (P=0.001). CONCLUSIONS: Positive remodeling and larger plaque areas were associated with unstable clinical presentation, whereas negative remodeling was more common in patients with stable clinical presentation. This association between the extent of remodeling and clinical presentation may reflect a greater tendency of plaques with positive remodeling to cause unstable coronary syndromes.

High prevalence of coronary atherosclerosis in asymptomatic teenagers and young adults: evidence from intravascular ultrasound.

BACKGROUND: Most of our knowledge about atherosclerosis at young ages is derived from necropsy studies, which have inherent limitations. Detailed, in vivo data on atherosclerosis in young individuals are limited. Intravascular ultrasonography provides a unique opportunity for in vivo characterization of early atherosclerosis in a clinically relevant context. METHODS AND RESULTS: Intravascular ultrasound was performed in 262 heart transplant recipients 30.9+/-13.2 days after transplantation to investigate coronary arteries in young asymptomatic subjects. The donor population consisted of 146 men and 116 women (mean age of 33.4+/-13.2 years). Extensive imaging of all possible (including distal) coronary segments was performed. Sites with the greatest and least intimal thickness in each CASS segment were measured in multiple coronary arteries. Sites with intimal thickness >/=0.5 mm were defined as atherosclerotic. A total of 2014 sites within 1477 segments in 574 coronary arteries (2.2 arteries per person) were analyzed. An atherosclerotic lesion was present in 136 patients, or 51.9%. The prevalence of atherosclerosis varied from 17% in individuals <20 years old to 85% in subjects >/=50 years old. In subjects with atherosclerosis, intimal thickness and area stenosis averaged 1.08+/-0.48 mm and 32.7+/-15.9%, respectively. For all age groups, the average intimal thickness was greater in men than women, although the prevalence of atherosclerosis was similar (52% in men and 51.7% in women). CONCLUSIONS: This study demonstrates that coronary atherosclerosis begins at a young age and that lesions are present in 1 of 6 teenagers. These findings suggest the need for intensive efforts at coronary disease prevention in young adults.

Pronounced benefit of coronary stenting and adjunctive platelet glycoprotein IIb/IIIa inhibition in complex atherosclerotic lesions.

BACKGROUND: Previous trials testing stents compared with balloon angioplasty excluded patients with complex lesions and did not assess the effect of adjunctive platelet IIb/IIIa inhibition. This analysis sought to assess the effect of stenting and abciximab specifically for patients with complex lesions. METHODS AND RESULTS: Patients with complex lesions (long, tandem, severely calcified, restenotic, thrombotic, or ostial; total occlusions; bifurcations; saphenous vein grafts; and multivessel interventions) from the Evaluation of PTCA to Improve Long-Term Outcome by c7E3 GP IIb/IIIa Receptor Blockade (EPILOG) and the Evaluation of Platelet IIb/IIIa Inhibitor for Stenting (EPISTENT) trials were included in the analysis. The 1-year combined death or myocardial infarction rates in the 4 treatment groups were as follows: balloon angioplasty/placebo, 14.2%; stent/placebo, 15.8%; balloon angioplasty/abciximab, 7.6%; and stent/abciximab, 8.0% (P<0.001). Death rates were 3.2%, 3.1%, 2.1%, and 0.5%, respectively (P=0.03). The incidence of target vessel revascularization at 1 year was 30.5%, 18.0%, 24.4%, and 19.7% in the 4 groups, respectively (P<0.001). After adjustment for baseline differences, multivariate analysis demonstrated that the rate of death or myocardial infarction was independently reduced by balloon angioplasty/abciximab (hazard ratio, 0.51; P<0.001) and stent/abciximab (hazard ratio, 0.60; P=0.02) but was not affected by the use of stents alone. Conversely, target vessel revascularization was reduced by stent/placebo (hazard ratio, 0.53; P<0.001), stent/abciximab (hazard ratio, 0.58; P<0.001), and balloon angioplasty/abciximab (hazard ratio, 0.74; P=0.006) compared with balloon angioplasty/placebo, respectively. CONCLUSIONS: The combination of stenting and abciximab during percutaneous coronary interventions for patients with angiographically complex lesions confers additive long-term benefit with respect to death, myocardial infarction, and target vessel revascularization.

Elevated circulating levels of serum tumor necrosis factor-alpha in patients with hemodynamically significant pressure and volume overload.

OBJECTIVES: We sought to determine whether serum tumor necrosis factor-alpha (TNF-alpha) levels are elevated in patients with hemodynamically significant pressure and volume overload. BACKGROUND: It has been previously shown that TNF-alpha messenger ribonucleic acid (mRNA) and protein are rapidly expressed in the hearts of animal models subjected to abrupt hemodynamic overloading. The clinical significance of these experimental findings has not been tested in pathophysiologically relevant clinical models in human subjects. METHODS: We prospectively measured serum TNF-alpha levels and serum TNF receptor 1 and 2 levels in 21 patients with severe aortic stenosis (AS), in 26 patients with 3+ to 4+ mitral regurgitation (MR) and in normal age- and gender-matched control subjects. Patients with AS and MR were either in New York Heart Association (NYHA) functional class I or II and had no significant coronary disease. We compared the cytokine levels among the groups using analysis of variance. We related cytokine levels to the severity of AS using simple regression analysis. RESULTS: Serum TNF-alpha levels in patients with AS (2.1 +/- 1.6 pg/ml, n = 21) and MR (1.3 +/-0.7 pg/ml, n = 26) were significantly higher than those in the control subjects (0.7 +/-0.2 pg/ml, n = 28). Serum TNF receptor 1 and 2 levels were also higher in patients with AS and MR than in control subjects. Cytokine levels were higher in patients in NYHA class II than in those in class I. In patients with a normal ejection fraction (>50%, n = 16), there was a mild positive correlation (r = 0.56, p = 0.025) between serum TNF-alpha levels and the mean gradient across the aortic valve. CONCLUSIONS: This study demonstrates that serum TNF-alpha is elevated in patients with chronic hemodynamic overloading and early cardiac decompensation. Furthermore, these findings suggest not only that peripheral TNF-alpha levels correlate with the severity of the hemodynamic pressure overload, but also that peripheral TNF-alpha and TNF receptor levels increase in direct relation to deteriorating NYHA functional class.

Proinflammatory cytokine levels in patients with depressed left ventricular ejection fraction: a report from the Studies of Left Ventricular Dysfunction (SOLVD).

OBJECTIVES: This study sought to assess proinflammatory cytokine levels in patients in the studies of left ventricular dysfunction trial (SOLVD) in relation to both their New York Heart Association functional classification and their neurohormonal status before randomization. BACKGROUND: Elevated levels of tumor necrosis factor-alpha have been identified in 30% to 40% of patients with heart failure. However, it is unclear which subsets of patients with heart failure elaborate tumor necrosis factor-alpha. It is also unclear what the mechanism for the increased expression of proinflammatory cytokines is. METHODS: Tumor necrosis factor-alpha and interleukin-6 levels were analyzed by enzymes-linked immunoassay using randomly selected plasma samples from patients in functional classes I to III who were enrolled in neurohormonal substudies of the SOLVD trial; age-matched healthy subjects served as the control group. RESULTS: Plasma levels of tumor necrosis factor-alpha (p < 0.001) were elevated in patients in functional classes I to III ([mean +/- SD] 1.95 +/- 0.54, 2.63 +/- 0.48, 6.4 +/- 1.9 pg/ml, respectively) compared with age-matched control subjects (0.75 +/- 0.05 pg/ml) and were progressively elevated in relation to decreasing functional status of the patient. Plasma levels of interleukin-6 (p < 0.001) were elevated in patients in functional classes I to III (3.3 +/- 0.55, 6.2 +/- 1.1, 5.22 +/- 0.9 pg/ml, respectively) compared with age-matched control subjects (1.8 +/- 0.5 pg/ml and were progressively elevated in relation to decreasing functional status of the patient. Cox proportional-hazards analysis showed that there was a trend toward significance between plasma tumor necrosis factor-alpha (p < 0.07) and survival, whereas there was no significant relation for plasma interleukin-6 (p < 0.72). Except for atrial natriuretic factor, which correlated weakly (r = 0.23, p = 0.04) with circulating tumor necrosis factor-alpha levels, there was no significance correlation between neurohormonal and proinflammatory cytokine levels. CONCLUSIONS: Circulating levels of proinflammatory cytokines increase in patients as their functional heart failure classification deteriorates. Moreover, activation of the neurohumoral axis is unlikely to completely explain the elaboration of proinflammatory cytokines in heart failure.

Impact of lipid abnormalities in development and progression of transplant coronary disease: a serial intravascular ultrasound study.

OBJECTIVES: We sought to determine the role of conventional atherosclerosis risk factors in the development and progression of transplant coronary artery disease (CAD) using serial intravascular ultrasound imaging. BACKGROUND: Transplant artery disease is a combination of allograft vasculopathy and donor atherosclerosis. The clinical determinants for each of these disease processes are not well characterized. Intravascular ultrasound imaging is the most sensitive tool to serially study these processes. METHODS: Baseline intravascular ultrasound imaging was performed 0.9 +/- 0.5 months after transplantation to identify donor atherosclerosis. Follow-up imaging was performed at 1.0 +/- 0.07 year to evaluate progression of donor atherosclerosis and development of transplant vasculopathy. Conventional risk factors for CAD included recipient age, gender, smoking history, diabetes mellitus, hypertension and hypercholesterolemia. RESULTS: Donor-transmitted atherosclerosis was present in 36 patients (39%). At follow-up, progression of donor lesions was seen in 15 patients (42%) and 42 patients (45%) developed transplant vasculopathy, leaving 35 patients (38%) without any disease. There was no difference in any conventional risk factors in patients with and without allograft vasculopathy. However, the severity of allograft vasculopathy was associated with a larger increase in low density lipoprotein (LDL) cholesterol from baseline (p = 0.02). High one-year posttransplant serum triglyceride level and pretransplant body mass index were the only significant predictors (p = 0.03) for progression of donor atherosclerosis. CONCLUSIONS: Conventional atherosclerosis risk factors do not predict development of allograft vasculopathy, but greater change in serum LDL cholesterol level during the first year after transplant is associated with more severe vasculopathy. Therefore, maintenance of LDL cholesterol as close to pretransplant values as possible may help to limit the rate of progression of acquired allograft vasculopathy.

Outcome of patients with hypertrophic obstructive cardiomyopathy after percutaneous transluminal septal myocardial ablation and septal myectomy surgery.

OBJECTIVES: This study was conducted to evaluate follow-up results in patients with hypertrophic obstructive cardiomyopathy (HOCM) who underwent either percutaneous transluminal septal myocardial ablation (PTSMA) or septal myectomy. BACKGROUND: Controversy exists with regard to these two forms of treatment for patients with HOCM. METHODS: Of 51 patients with HOCM treated, 25 were treated by PTSMA and 26 patients via myectomy. Two-dimensional echocardiograms were performed before both procedures, immediately afterwards and at a three-month follow-up. The New York Heart Association (NYHA) functional class was obtained before the procedures and at follow-up. RESULTS: Interventricular septal thickness was significantly reduced at follow-up in both groups (2.3 +/- 0.4 cm vs. 1.9 +/- 0.4 cm for septal ablation and 2.4 +/- 0.6 cm vs. 1.7 +/- 0.2 cm for myectomy, both p < 0.001). Estimated by continuous-wave Doppler, the resting pressure gradient (PG) across the left ventricular outflow tract (LVOT) significantly decreased immediately after the procedures in both groups (64 +/- 39 mm Hg vs. 28 +/- 29 mm Hg for PTSMA, 62 +/- 43 mm Hg vs. 7 +/- 7 mm Hg for myectomy, both p < 0.0001). At three-month follow-up, the resting PG remained lower in the PTSMA and myectomy groups (24 +/- 19 mm Hg and 11 +/- 6 mm Hg, respectively, vs. those before procedures, both p < 0.0001). The NYHA functional class was also significantly improved in both groups (3.5 +/- 0.5 vs. 1.9 +/- 0.7 for PTSMA, 3.3 +/- 0.5 vs. 1.5 +/- 0.7 for myectomy, both p < 0.0001). CONCLUSIONS: Both myectomy and PTSMA reduce LVOT obstruction and significantly improve NYHA functional class in patients with HOCM. However, there are benefits and drawbacks for each therapeutic method that must be counterbalanced when deciding on treatment for LVOT obstruction.

Effect of aspirin on phase gradient of 2F1-F2 distortion product otoacoustic emissions.

It is well known that aspirin consumption temporarily reduces overall otoacoustic emission (OAE) amplitude in humans. However, little is known about changes in the separate components of distortion product otoacoustic emissions (DPOAE), which may be distinguished by examining phase gradients. The effects of aspirin on the phase gradient of the DPOAE 2F1-F2 obtained with fixed frequency ratio sweeps were studied longitudinally in a group of twelve subjects in whom a temporary hearing loss was induced by aspirin consumption. DPOAE were recorded daily for two days pre-aspirin consumption, during the three days of aspirin consumption and two days afterwards. DP-grams were recorded over a restricted frequency range centered on 2,3,4 and 6 kHz with the following stimulus levels: L1/L2 of 60/50-80/70 in 10-dB steps. The effects of aspirin on the phase gradients varied between the subjects and across frequency: the general trend was that the phase gradient became steeper across successive sessions for the higher frequencies, while no significant effect was found at the lower frequencies. These results suggest that aspirin may have more persistent effects on cochlear function than are disclosed by measurements of hearing threshold level or DPOAE amplitude. Particularly, DPOAE phase gradient appears to be increased by aspirin consumption and has not recovered two days after cessation of aspirin intake, despite almost complete recovery of DPOAE amplitude and hearing threshold levels. These findings may suggest differential effects on the distortion and reflection mechanisms considered to underlie DPOAE generation.

Tuberculous bacillemia, hyperpyrexia, and rapid death.

Hyperpyrexia, followed rapidly by multiple organ failure and death, developed in a previously healthy man. Postmortem examination indicated disseminated tuberculosis with adrenal involvement, but also evidence compatible with heat stroke. Mycobacterium tuberculosis was isolated from a routine blood culture. The patient's symptoms may have been the result of his bacillemia or the result of unapparent tuberculous chronic adrenocortical insufficiency that made him unusually sensitive to heat.

Regulation of CD34 expression in differentiating M1 cells.

CD34 is a cell surface glycoprotein expressed on hematopoietic stem and progenitor cells, but not on mature blood cells. In the present study we found that CD34 downregulation during hematopoiesis occured at the level of transcriptional initiation. Two transcription initiation sites (TISs) were identified in each of three different CD34+ cell lines; these TISs were located at 120 and 80 bp 5' of the translation start site, respectively. The promoter lacks TATA elements and, like other TATA-less promoters, the TISs conform to the consensus sequence for an INR (PyPyCAPyPyPyPy). An additional 3000 bp of upstream genomic DNA were sequenced and found to contain consensus sites for transcription factors, suggesting their potential role in gene regulation. Transient transfection assays using CD34 promoter-luciferase reporter constructs, containing sequences up to 3 kb upstream and inclusive of the TIS, indicate that this promoter drives transcription in hematopoietic CD34+ cells but not CD34+ nonhematopoietic cells. Both cell type specific expression and full promoter activity are maintained in constructs that contain as little as 454 bp upstream of the TISs. Optimal promoter activity requires the 5' untranslated region of exon 1, which contains a 51-bp element that has the potential to form an extensive secondary structure. In the plasmid DNA, however, this secondary structure was not detectable by P1 nuclease digestion. At least three proteins present in uninduced M1 nuclear extracts bind to this element. Two of the three proteins were identified as Sp 1 and Sp 3 based on supershift experiments. These data suggest that CD34 expression by hematopoietic stem and progenitor cells involves hematopoietic cell-specific factors that interact with regulatory elements within the first 230 bp of the promoter and that optimal expression requires a 60-bp segment of the 5' untranslated region.

Targeted expression of calcitonin gene-related peptide to osteoblasts increases bone density in mice.

The neuropeptide calcitonin gene-related peptide (CGRP) is concentrated in fine sensory nerve endings innervating all tissues, including bone. CGRP inhibits osteoclasts, stimulates insulin-like growth factor I and inhibits tumor necrosis factor alpha production by osteoblasts in vitro. To investigate the role of CGRP in bone in vivo, mice were engineered to express CGRP in osteoblasts by placing the human CGRP gene under the control of the rat osteocalcin promoter (Ost-CGRP tg+ mice). Calvaria cultures from transgene positive (tg+), but not tg- mice, produced bioactive CGRP. Trabecular bone density and bone volume, determined by peripheral quantitative computed tomography and bone histomorphometry, respectively, were higher in tg+ than tg- littermates. This increase in bone volume was associated with an increased bone formation rate. Trabecular bone density decreased in tg+ mice as a result of ovariectomy, but remained higher than in sham tg- mice. Targeting CGRP to osteoblasts appears to favor the establishment of a higher trabecular bone mass in mice.

Initial experience of platelet glycoprotein IIb/IIIa inhibition with abciximab during carotid stenting: a safe and effective adjunctive therapy.

BACKGROUND AND PURPOSE: Abciximab has been shown to decrease periprocedural ischemic complications after coronary intervention. However, the adjunctive use of abciximab in carotid stenting has not been adequately studied. We sought to determine the efficacy and safety of abciximab in carotid stenting. METHODS: Carotid stenting was performed in 151 consecutive patients determined to be at high surgical risk by a vascular surgeon. Of these, 128 consecutive patients received adjuvant therapy with abciximab (0.25 mg/kg bolus before the lesion was crossed with guidewire and 0.125 micro. kg(-1). min(-1) infusion for 12 hours.). A heparin bolus of 50 U/kg was given, and activated clotting time was maintained between 250 to 300 seconds. All patients received aspirin and thienopyridine. Procedural and 30-day outcomes were compared between the control (n=23) and abciximab (n=128) groups. RESULTS: The 2 groups had similar baseline characteristics. Procedural events were more frequent in the control group (8%; 1 major stroke and 1 neurological death) compared with the abciximab group (1.6%; 1 minor stroke and 1 retinal infarction; P=0.05). On 30-day follow-up, 1 patient presented with delayed intracranial hemorrhage in the abciximab group. There were no other major bleeding complications. CONCLUSIONS: Adjunctive use of abciximab for carotid stenting is safe with no increase in the risk of intracranial hemorrhage. This adjunctive therapy with potent glycoprotein IIb/IIIa inhibition may help to reduce periprocedural adverse events in patients undergoing carotid stenting.