bluuebunny/crossref_metadata_2025_split huggingface dataset:
Volume-based referral for cardiovascular procedures in the United States: a cross-sectional regression analysis
Authors: Epstein Andrew J , Rathore Saif S , Krumholz Harlan M , Volpp Kevin GM 
Published: June 2005

Abstract

Background
We sought to estimate the numbers of patients affected and deaths avoided by adopting the Leapfrog Group's recommended hospital procedure volume minimums for coronary artery bypass graft (CABG) surgery and percutaneous coronary intervention (PCI). In addition to hospital risk-adjusted mortality standards, the Leapfrog Group recommends annual hospital procedure minimums of 450 for CABG and 400 for PCI to reduce procedure-associated mortality.

Methods
We conducted a retrospective analysis of a national hospital discharge database to evaluate in-hospital mortality among patients who underwent PCI (n = 2,500,796) or CABG (n = 1,496,937) between 1998 and 2001. We calculated the number of patients treated at low volume hospitals and simulated the number of deaths potentially averted by moving all patients to high volume hospitals under best-case conditions (i.e., assuming the full volume-associated reduction in mortality and the capacity to move all patients to high volume hospitals with no related harms).

Results
Multivariate adjusted odds of in-hospital mortality were higher for patients treated in low volume hospitals compared with high volume hospitals for CABG (OR 1.16, 95% CI 1.10–1.24) and PCI (OR 1.12, 95% CI 1.05–1.20). A policy of hospital volume minimums would have required moving 143,687 patients for CABG and 87,661 patients for PCI from low volume to high volume hospitals annually and prevented an estimated 619 CABG deaths and 109 PCI deaths. Thus, preventing a single death would have required moving 232 CABG patients or 805 PCI patients from low volume to high volume hospitals.

Conclusion
Recommended hospital CABG and PCI volume minimums would prevent 728 deaths annually in the United States, fewer than previously estimated. It is unclear whether a policy requiring the movement of large numbers of patients to avoid relatively few deaths is feasible or effective.
Comparison of rosuvastatin and atorvastatin for lipid lowering in patients with type 2 diabetes mellitus: results from the URANUS study
Authors: Berne Christian , Siewert-Delle Annica ,   the URANUS study investigators
Published: June 2005

AbstractObjectiveThe Use of Rosuvastatin versus Atorvastatin iN type 2 diabetes mellitUS (URANUS) study compared rosuvastatin with atorvastatin for the reduction of low-density lipoprotein cholesterol (LDL-C) in patients with type 2 diabetes.MethodsAfter a 6-week dietary run-in, patients aged ≥ 18 years with type 2 diabetes and LDL-C ≥ 3.3 mmol/L were randomised to double-blind treatment with rosuvastatin 10 mg (n = 232) or atorvastatin 10 mg (n = 233) for 4 weeks. Doses were then titrated up to a maximum of rosuvastatin 40 mg or atorvastatin 80 mg over 12 weeks to achieve the 1998 European LDL-C goal (<3.0 mmol/L).ResultsRosuvastatin reduced LDL-C levels significantly more than atorvastatin during the fixed-dose and titration periods (p < 0.0001). Significantly more patients reached the 1998 LDL-C goal with rosuvastatin 10 mg compared with atorvastatin 10 mg at 4 weeks (81% vs 65%, p < 0.001). At 16 weeks, significantly more patients achieved their LDL-C goal with rosuvastatin compared with atorvastatin (94% vs 88%, p < 0.05) and more patients receiving rosuvastatin remained at their starting dose with reduced requirement for dose titration. At 4 weeks, 65% of rosuvastatin patients had reached their 2003 European LDL-C goal (< 2.5 mmol/L), compared with 33% of atorvastatin patients (p < 0.0001). Both treatments were similarly well tolerated with no unexpected safety concerns.ConclusionAt the start dose and following dose titration, rosuvastatin was significantly more effective than atorvastatin at reducing LDL-C and achieving European LDL-C goals in patients with type 2 diabetes.
Replacing a Swiss ball for an exercise bench causes variable changes in trunk muscle activity during upper limb strength exercises
Authors: Lehman Gregory J , Gordon Trish , Langley Jo , Pemrose Patricia , Tregaskis Sara 
Published: June 2005

Abstract
Background
The addition of Swiss balls to conventional exercise programs has recently been adopted. Swiss balls are an unstable surface which may result in an increased need for force output from trunk muscles to provide adequate spinal stability or balance. The aim of the study was to determine whether the addition of a Swiss ball to upper body strength exercises results in consistent increases in trunk muscle activation levels.

Methods
The myoelectric activity of four trunk muscles was quantified during the performance of upper body resistance exercises while seated on both a stable (exercise bench) and labile (swiss ball) surface. Participants performed the supine chest press, shoulder press, lateral raise, biceps curl and overhead triceps extension. A repeated measures ANOVA with post-hoc Tukey test was used to determine the influence of seated surface type on muscle activity for each muscle.

Results & Discussion
There was no statistically significant (p < .05) difference in muscle activity between surface conditions. However, there was large degree of variability across subjects suggesting that some individuals respond differently to surface stability. These findings suggest that the incorporation of swiss balls instead of an exercise bench into upper body strength training regimes may not be justified based only on the belief that an increase spinal stabilizing musculature activity is inherent. Biomechanically justified ground based exercises have been researched and should form the basis for spinal stability training as preventative and therapeutic exercise training regimes.

Conclusion
Selected trunk muscle activity during certain upper limb strength training exercises is not consistently influenced by the replacement of an exercise bench with a swiss ball.
Soluble HLA measurement in saliva and cerebrospinal fluid in Caucasian patients with multiple sclerosis: a preliminary study
Authors: Adamashvili Irena , Minagar Alireza , Gonzalez-Toledo Eduardo , Featherston Liubov , Kelley Roger E 
Published: June 2005

AbstractBackgroundMeasurement of soluble HLA in body fluids has a potential role in assessing disease activity in autoimmune disorders.MethodsWe applied a solid phase, enzyme-linked immunoassay to measure soluble HLA class I (sHLA-I) and class II (sHLA-II) molecules in the saliva and cerebrospinal fluid (CSF) in 13 untreated patients with relapsing-remitting form of multiple sclerosis (MS). For comparison purposes, we also studied saliva from 53 healthy subjects.ResultsSaliva from normal controls had detectable sHLA-I levels in 41 of 53 individuals studied, with values ranging from 9–100 ng/ml (mean = 41 ± 2.8 ng/ml). sHLA-I was undetectable in the saliva in 11 of 13 MS patients, and in none of the CSF specimens. In contrast, mean sHLA-II concentration in the saliva of MS patients was significantly increased compared to controls (386 ± 52 unit/ml vs. 222 ± 18.4 unit/ml, t = 8.68, P < 0.005). The mean CSF sHLA-II level (369 ± 16 unit/ml) was equivalent to the mean sHLA-II concentration measured in saliva (mean = 386 ± 52 unit/ml) (P = 0.7). In patients with brain magnetic resonance imaging (MRI) enhancing lesions (n = 5), reflective of more active disease, CSF sHLA-II averaged 356 ± 26 unit/ml compared to 380 ± 51 in saliva. Similarly, in patients with non-enhancing lesions (n = 8), CSF sHLA-II averaged 377 ± 18 unit/ml compared to 390 ± 77 unit/ml in saliva. Thus, the mean sHLA-II concentration in saliva and CSF was essentially equivalent for MS patients with or without enhancing plaques.ConclusionOur data suggest that the measurement of soluble HLA in saliva, specifically sHLA-II, correlates with the level found in the CSF. Therefore, if sHLA correlates with disease activity in MS, as has been proposed, saliva measurements provide a noninvasive correlate of CSF measurement.
Somatic mutation and gain of copy number of PIK3CA in human breast cancer
Authors: Wu Guojun , Xing Mingzhao , Mambo Elizabeth , Huang Xin , Liu Junwei , Guo Zhongmin , Chatterjee Aditi , Goldenberg David , Gollin Susanne M , Sukumar Saraswati , Trink Barry , Sidransky David 
Published: May 2005

Abstract
Introduction
Phosphatidylinositol 3-kinases (PI3Ks) are a group of lipid kinases that regulate signaling pathways involved in cell proliferation, adhesion, survival, and motility. Even though PIK3CA amplification and somatic mutation have been reported previously in various kinds of human cancers, the genetic change in PIK3CA in human breast cancer has not been clearly identified.

Methods
Fifteen breast cancer cell lines and 92 primary breast tumors (33 with matched normal tissue) were used to check somatic mutation and gene copy number of PIK3CA. For the somatic mutation study, we specifically checked exons 1, 9, and 20, which have been reported to be hot spots in colon cancer. For the analysis of the gene copy number, we used quantitative real-time PCR and fluorescence in situ hybridization. We also treated several breast cancer cells with the PIK3CA inhibitor LY294002 and compared the apoptosis status in cells with and without PIK3CA mutation.

Results
We identified a 20.6% (19 of 92) and 33.3% (5 of 15) PIK3CA somatic mutation frequency in primary breast tumors and cell lines, respectively. We also found that 8.7% (8 of 92) of the tumors harbored a gain of PIK3CA gene copy number. Only four cases in this study contained both an increase in the gene copy number and a somatic mutation. In addition, mutation of PIK3CA correlated with the status of Akt phosphorylation in some breast cancer cells and inhibition of PIK3CA-induced increased apoptosis in breast cancer cells with PIK3CA mutation.

Conclusion
Somatic mutation rather than a gain of gene copy number of PIK3CA is the frequent genetic alteration that contributes to human breast cancer progression. The frequent and clustered mutations within PIK3CA make it an attractive molecular marker for early detection and a promising therapeutic target in breast cancer.
Comparison of post-disaster psychiatric disorders after terrorist bombings in Nairobi and Oklahoma City
Authors: North Carol S. , Pfefferbaum Betty , Narayanan Pushpa , Thielman Samuel , McCoy Gretchen , Dumont Cedric , Kawasaki Aya , Ryosho Natsuko , Spitznagel Edward L. 
Published: May 2005

BackgroundAfrican disaster-affected populations are poorly represented in disaster mental health literature.AimsTo compare systematically assessed mental health in populations directly exposed to terrorist bombing attacks on two continents, North America and Africa.MethodStructured diagnostic interviews compared citizens exposed to bombings of the US Embassy in Nairobi, Kenya (n=227) and the Oklahoma City Federal Building (n=182).ResultsPrevalence rates of post-traumatic stress disorder (PTSD) and major depression were similar after the bombings. No incident (new since the bombing) alcohol use disorders were observed in either site. Symptom group C was strongly associated with PTSD in both sites. The Nairobi group relied more on religious support and the Oklahoma City group used more medical treatment, drugs and alcohol.ConclusionsPost-disaster psycho-pathology had many similarities in the two cultures; however, coping responses and treatment were quite different. The findings suggest potential for international generalisability of post-disaster psychopathology, but confirmatory studies are needed.
Gonadotropin-Releasing Hormone I Analog Acts as an Antiapoptotic Factor in Mouse Blastocysts
Authors: Kawamura Kazuhiro , Fukuda Jun , Kumagai Jin , Shimizu Yasushi , Kodama Hideya , Nakamura Akira , Tanaka Toshinobu 
Published: June 2005

AbstractBoth GnRH-I and its receptor (GnRHR)-I have been shown to be expressed in the mammalian preimplantation embryo. In this study, we investigated the molecular mechanisms of GnRH-I in the regulation of early embryonic development in mouse. We found that GnRH-I and GnRHR-I mRNAs were detectable throughout early embryonic stages and that expression levels of both increased significantly after the early blastocyst stage. In blastocysts, GnRH-I and GnRHR-I expression was detected in both inner cell mass and trophectoderm cells. The pregnant uterus also expressed both genes, suggesting that preimplantation embryos could be affected by GnRH through both paracrine and autocrine signaling. Treatment with GnRH-I agonist, buserelin, promoted development of two-cell-stage embryos to the expanded and hatched blastocyst stages and inhibited apoptosis in a dose-dependent manner. In contrast, treatment with GnRH-I antagonist, ganirelix acetate, inhibited development of preimplantation embryos beyond the expanded blastocyst stage and induced apoptosis; both effects could be reversed by cotreatment with GnRH-I agonist. GnRH-I antagonist-induced cell death was mediated by disruption of mitochondrial function, release of cytochrome c, and activation of caspase-3. Furthermore, treatment with GnRH-I antagonist decreased expression of two antiapoptotic growth factors, epidermal growth factor and IGF-II, in blastocysts. These results indicate that GnRH-I, acting as an antiapoptotic factor, is an important growth factor in development of mouse blastocysts.
The Effect of the Melanocortin Agonist, MT-II, on the Defended Level of Body Adiposity
Authors: Seeley Randy J. , Burklow Melissa L. , Wilmer Kihmberly A. , Matthews Colette C. , Reizes Ofer , McOsker Charles C. , Trokhan Darren P. , Gross Marla C. , Sheldon Russell J. 
Published: June 2005

Abstract
A wide range of experimental evidence implicates a critical role for melanocortin signaling in the control of food intake and body adiposity. Melanocortin receptor agonists such as MT-II potently reduce food intake and body weight, making such agonists potential therapeutics for obesity. The critical concept addressed by the present experiments is whether the homeostatic effects of melanocortin agonists directly regulate food intake or whether the effects on food intake are secondary, with the primary effects being the regulation of body weight and adiposity. To investigate this, we compared the effect of various doses of MT-II given via osmotic minipump for 28 d to alter food intake, body weight, and body fat in dietary-induced obese rats. In addition, before the implantation of the minipump, dietary-induced obese rats were weight reduced by differing amounts using varying levels of food restriction. The results show that in food-restricted rats, MT-II-treated rats consume significantly more calories than those receiving MT-II after ad libitum access to food. More importantly, regardless of the widely differing levels of body fat among the different dietary treatments employed, body fat at the end of the study was determined exclusively by the dose of MT-II, with MT-II-treated rats having less body fat than vehicle-treated rats. These experiments support the hypothesis that melanocortin signaling primarily regulates total body adiposity and that food intake is adjusted as necessary to achieve a specific level of body adiposity.
Peripheral Exendin-4 and Peptide YY3–36 Synergistically Reduce Food Intake through Different Mechanisms in Mice
Authors: Talsania Tanvi , Anini Younes , Siu Stephanie , Drucker Daniel J. , Brubaker Patricia L. 
Published: June 2005

AbstractGlucagon-like peptide-17–36NH2 (GLP-1) and peptide YY3–36NH2 (PYY3–36NH2) are cosecreted from the intestine in response to nutrient ingestion. Peripheral administration of GLP-1 or PYY3–36NH2 decreases food intake (FI) in rodents and humans; however, the exact mechanisms by which these peptides regulate FI remain unclear. Male C57BL/6 mice were injected (ip) with exendin-41–39 (Ex4, a GLP-1 receptor agonist) and/or PYY3–36NH2 (0.03–3 μg), and FI was determined for up to 24 h. Ex4 and PYY3–36NH2 alone decreased FI by up to 83 and 26%, respectively (P &lt; 0.05–0.001), whereas a combination of the two peptides (0.06 μg Ex4 plus 3 μg PYY3–36NH2) further reduced FI for up to 8 h in a synergistic manner (P &lt; 0.05–0.001). Ex4 and/or PYY3–36NH2 delayed gastric emptying by a maximum of 19% (P &lt; 0.01–0.001); however, there was no significant effect on locomotor activity nor was there induction of taste aversion. Capsaicin pretreatment prevented the inhibitory effect of Ex4 on FI (P &lt; 0.05), but had no effect on the anorexigenic actions of PYY3–36NH2. Similarly, exendin-49–39 (a GLP-1 receptor antagonist) partially abolished Ex4-induced anorexia (P &lt; 0.05), but did not affect the satiation produced by PYY3–36NH2. Conversely, BIIE0246 (a Y2 receptor antagonist) completely blocked the anorexigenic effects of PYY3–36NH2 (P &lt; 0.001), but had no effect on Ex4-induced satiety. Thus, Ex4 and PYY3–36NH2 suppress FI via independent mechanisms involving a GLP-1 receptor-dependent, sensory afferent pathway (Ex4) and a Y2-receptor mediated pathway (PYY3–36NH2). These findings suggest that administration of low doses of Ex4 together with PYY3–36NH2 may increase the suppression of FI without inducing significant side effects.
Carotid Angioplasty with or without Stent Placement versus Carotid Endarterectomy for Treatment of Carotid Stenosis: A Meta-analysis
Authors: Qureshi Adnan I. , Kirmani Jawad F. , Divani Afshin A. , Hobson Robert W. 
Published: May 2005

AbstractOBJECTIVE:Carotid angioplasty with or without stent placement (CAS) has been proposed as an alternative method to carotid endarterectomy (CEA) for treatment of carotid stenosis. Small randomized trials have evaluated the comparative efficacy of both methods; however, definitive evidence is lacking.METHODS:A search was made for randomized clinical trials comparing CAS and CEA for treatment of carotid stenosis. A literature search of MEDLINE, PubMed, and Cochrane databases was supplemented by a review of bibliographies of relevant articles and personal files. A meta-analysis was performed using a random effects model because significant heterogeneity was observed. Outcomes compared included 1-month composite rates of stroke or death, all strokes, disabling strokes, myocardial infarction, cranial nerve injury, and major bleeding and 1-year rates of both minor and major ipsilateral strokes.RESULTS:We analyzed five randomized trials totaling 1154 patients (577 randomized to CEA and 577 randomized to CAS). The composite end point of 1-month stroke or death rate was not different between patients treated with CAS compared with those treated with CEA (relative risk [RR], 1.3; 95% confidence interval [CI], 0.6–2.8; P = 0.5). The 1-month stroke rate (831 patients analyzed: RR, 1.3; 95% CI, 0.4–3.6; P = 0.7) and disabling stroke rate (831 patients analyzed: RR, 0.9; 95% CI, 0.2–3.5; P = 0.9) was similar for CAS and CEA. The 1-month rates of myocardial infarction (814 patients analyzed: RR, 0.3; 95% CI, 0.1–0.9) and cranial nerve injury (918 patients analyzed: RR, 0.05; 95% CI, 0.01–0.3) were significantly lower for CAS. No significant differences were observed in 1-year rates of ipsilateral stroke (814 patients analyzed: RR, 0.8; 95% CI, 0.5–1.2; P = 0.2).CONCLUSION:The 30-day stroke and death rates associated with CAS and CEA were not significantly different. Lower rates of myocardial infarction and cranial nerve injury were observed with CAS compared with CEA.
Brainstem Cavernomas: Long-term Results of Microsurgical Resection in 52 Patients
Authors: Ferroli Paolo , Sinisi Marco , Franzini Angelo , Giombini Sergio , Solero Carlo Lazzaro , Broggi Giovanni 
Published: May 2005

Abstract

OBJECTIVE:
To review the natural history and the long-term results of microsurgical resection of brainstem cavernous angiomas operated on in one institution.

METHODS:
A retrospective analysis was conducted of the preoperative and postoperative course in 52 consecutive patients who underwent microsurgical resection of a brainstem cavernoma between 1990 and 2002. The role of sex, age, cavernoma location, size, multiple bleedings, relationships to the pial-ependymal surface, surgical approach, and preoperative magnetic resonance imaging appearance were evaluated as prognostic factors possibly influencing outcome. Discrete data were compared by use of the χ2 test and Fisher's exact test as appropriate.

RESULTS:
The risk of hemorrhage was 3.8% per patient per year. The rebleeding rate was 34.7%. Nineteen of 29 patients who experienced new neurological deficits after surgery improved over time to their preoperative condition or better. Permanent morbidity was observed in 10 (19%) of 52 patients (follow-up: 1.5–10.5 yr; mean, 4.7 yr; median, 4.3 yr; standard deviation, 0.2 yr). The final Karnofsky Performance Scale score for these 10 patients was 90 in 2 patients, 80 in 2, 70 in 2, 60 in 2, 50 in 1, and 30 in 1. The mortality rate was 1.9%. The incidence of permanent new neurological deficits was lower in the 20 patients whose lesion could be removed through an anterolateral pontine approach (5 versus 29%; P = 0.035).

CONCLUSION:
Surgical resection is recommended for superficial lesions and for lesions that can be reached through the anterolateral pontine surface. Surgery is also recommended for symptomatic cavernomas with a satellite subacute hematoma.
Usefulness of the Neuroform Stent for the Treatment of Cerebral Aneurysms: Results at Initial (3–6-mo) Follow-up
Authors: Fiorella David , Albuquerque Felipe C. , Deshmukh Vivek R. , McDougall Cameron G. 
Published: May 2005

Abstract

OBJECTIVE:
The Neuroform microstent, a flexible, self-expanding, nitinol stent specifically designed for use in the cerebral vasculature, became available in North America for aneurysm treatment in November 2002. The present report details our experience with the Neuroform stent over the past 2 years, with an emphasis on evolving treatment strategies and treatment durability at initial (3–6 mo) follow-up.

METHODS:
All patients included in this report were registered in a prospectively maintained database. We assessed the clinical history, indications for stent use, aneurysm dimensions, technical details of the procedures, degree of aneurysm occlusion, angiographic and clinical findings at follow-up, and complications.

RESULTS:
Over a 20-month period, 64 patients with 74 aneurysms were treated with 86 Neuroform stents. Of 64 patients, 16 (25%) were treated in the context of subarachnoid hemorrhage (8 acute, 7 subacute, 1 remote). Indications for stent use included broad aneurysm neck (n = 51 stents; average neck, 5.1 mm; aneurysm size, 8.2 mm), fusiform/dissecting morphology (n = 17), salvage/bailout for coils prolapsed into the parent vessel (n = 7), and giant aneurysm (n = 11). Sixty-one aneurysms were stented and coiled with complete or near complete (&gt;95%) occlusion in 28 patients (45.9%) and partial occlusion (&lt;95%) in 33 patients (54%). Follow-up angiographic (n = 43) or magnetic resonance angiographic (n = 5) data (average follow-up, 4.6 mo; median, 4 mo; range, 1.5–13 mo) for 48 aneurysms (46 patients) after stent-supported coil embolization demonstrated progressive thrombosis in 25 patients (52%), recanalization in 11 patients (23%) (8 of whom were retreated), and no change in 12 patients (25%). Follow-up angiography in 5 additional patients with dissecting aneurysms treated with stents alone demonstrated interval vascular remodeling with decreased aneurysm size in all patients. Delayed, severe, in-stent stenosis was observed in 3 patients, 1 of whom was symptomatic and required angioplasty and subsequently superficial temporal artery-to-middle cerebral artery bypass surgery. Using the second-generation Neuroform2 delivery system (n = 53), very few technical problems with stent delivery and deployment have been encountered (n = 2).

CONCLUSION:
The Neuroform stent facilitates adequate embolization of complex cerebral aneurysms, which would not otherwise be amenable to endovascular therapy. Initial follow-up data indicate favorable progressive thrombosis and recanalization rates for aneurysms after Neuroform stent-assisted embolization. These advantages of stenting were most evident for small aneurysms with wide necks.