bluuebunny/crossref_metadata_2025_split huggingface dataset:
Effects of polyethylene‐grafted maleic anhydride (PE‐g‐MA) on thermal properties, morphology, and tensile properties of low‐density polyethylene (LDPE) and corn starch blends
Authors: Liu W. , Wang Y.‐J. , Sun Z. 
Published: April 2003

AbstractThe effects of polyethylene‐grafted maleic anhydride (PE‐g‐MA) on the thermal properties, morphology, and tensile properties of blends of low‐density polyethylene (LDPE) and corn starch were studied with a differential scanning calorimeter (DSC), scanning electron microscope (SEM), and Instron Universal Testing Machine, respectively. Corn starch–LDPE blends with different starch content and with or without the addition of PE‐g‐MA were prepared with a lab‐scale twin‐screw extruder. The crystallization temperature of LDPE–corn starch–PE‐g‐MA blends was similar to that of pure LDPE but higher than that of LDPE–corn starch blends. The interfacial properties between corn starch and LDPE were improved after PE‐g‐MA addition, as evidenced by the structure morphology revealed by SEM. The tensile strength and elongation at break of corn starch–LDPE–PE‐g‐MA blends were greater than those of LDPE–corn starch blends, and their differences became more pronounced at higher starch contents. © 2003 Wiley Periodicals, Inc. J Appl Polym Sci 88: 2904–2911, 2003
Disruption of tumor necrosis factor receptor p55 impairs collagen turnover in experimentally induced sclerodermic skin fibroblasts
Authors: Murota Hiroyuki , Hamasaki Youichiro , Nakashima Tomoki , Yamamoto Kazuo , Katayama Ichiro , Matsuyama Toshifumi 
Published: April 2003

AbstractObjectiveTo determine the role of tumor necrosis factor receptor p55 (TNFRp55)–mediated signaling in the pathogenesis of scleroderma.MethodsA murine model of scleroderma that closely resembles systemic sclerosis in humans was used. Wild‐type and TNFRp55‐deficient (TNFRp55−/−) mice received a subcutaneous injection of bleomycin each day. The extent of skin fibrosis was determined by measurements of the dermal thickness, as well as histologic examinations. Expression levels of fibrogenic cytokines, procollagen α1, and matrix metalloproteinase 1 (MMP‐1), MMP‐2, and MMP‐9 messenger RNA (mRNA) were analyzed, both in vivo and in vitro, by reverse transcriptase–polymerase chain reaction assay or Western blotting.ResultsTNFRp55−/− mice began to develop severe sclerotic changes of the dermis on day 3 of the subcutaneous injections of bleomycin, while wild‐type mice did not. The expression levels of fibrogenic cytokines, procollagen α1, and MMP‐2 and MMP‐9 mRNA were unaffected in the skin of both wild‐type and TNFRp55−/− mice, with or without bleomycin treatment. Induction of MMP‐1 expression was significantly inhibited in the skin from bleomycin‐treated TNFRp55−/− mice, and this phenomenon was also observed in vitro.ConclusionThese results indicated that signaling mediated by TNFRp55 plays an essential role in MMP‐1 expression and a key role in the collagen degradation process in this murine model. This study might provide a basis for understanding the pathogenesis of scleroderma and formulating therapeutic intervention.
Prevalence of rheumatoid arthritis in persons 60 years of age and older in the United States: Effect of different methods of case classification
Authors: Rasch Elizabeth K. , Hirsch Rosemarie , Paulose‐Ram Ryne , Hochberg Marc C. 
Published: April 2003

AbstractObjectiveTo determine prevalence estimates for rheumatoid arthritis (RA) in noninstitutionalized older adults in the US. Prevalence estimates were compared using 3 different classification methods based on current classification criteria for RA.MethodsData from the Third National Health and Nutrition Examination Survey (NHANES‐III) were used to generate prevalence estimates by 3 classification methods in persons 60 years of age and older (n = 5,302). Method 1 applied the “n of k” rule, such that subjects who met 3 of 6 of the American College of Rheumatology (ACR) 1987 criteria were classified as having RA (data from hand radiographs were not available). In method 2, the ACR classification tree algorithm was applied. For method 3, medication data were used to augment case identification via method 2. Population prevalence estimates and 95% confidence intervals (95% CIs) were determined using the 3 methods on data stratified by sex, race/ethnicity, age, and education.ResultsOverall prevalence estimates using the 3 classification methods were 2.03% (95% CI 1.30–2.76), 2.15% (95% CI 1.43–2.87), and 2.34% (95% CI 1.66–3.02), respectively. The prevalence of RA was generally greater in the following groups: women, Mexican Americans, respondents with less education, and respondents who were 70 years of age and older.ConclusionThe prevalence of RA in persons 60 years of age and older is ∼2%, representing the proportion of the US elderly population who will most likely require medical intervention because of disease activity. Different classification methods yielded similar prevalence estimates, although detection of RA was enhanced by incorporation of data on use of prescription medications, an important consideration in large population surveys.
Risk of malignant lymphomas in patients with rheumatoid arthritis and in their first‐degree relatives
Authors: Ekström Karin , Hjalgrim Henrik , Brandt Lena , Baecklund Eva , Klareskog Lars , Ekbom Anders , Askling Johan 
Published: April 2003

AbstractObjectivePatients with rheumatoid arthritis (RA) are at increased risk for malignant lymphomas. Both conditions display a familial aggregation, and there are reports of RA and malignant lymphomas occurring in the same families. This study was undertaken to determine the risk of malignant lymphomas in first‐degree relatives of RA patients, in order to investigate whether the increased risk of malignant lymphomas in RA could be due to genetic or environmental risk factors common to both conditions, rather than being a consequence of the rheumatic disease.MethodsUsing Swedish nationwide and population‐based registers, we identified 76,527 patients hospitalized with RA in 1964–1999 and 70,290 first‐degree relatives of a subset of these patients. These subjects were followed up for more than 3 decades, and information on cancer occurrence was recorded.ResultsPatients with RA had a significantly increased risk of malignant lymphomas (535 cases; standardized incidence ratio [SIR] 2.00, 95% confidence interval [95% CI] 1.83–2.17), which was apparent for up to 2 decades of followup. Among the first‐degree relatives without RA, no increased risk of malignant lymphomas was found overall, although modest and nonsignificantly elevated risk estimates were observed in subgroups. With respect to childhood cancer (0–14 years of age), we observed an increased risk of Hodgkin's lymphoma (5 cases; SIR 3.18, 95% CI 1.03–7.42).ConclusionPatients with RA are at a markedly, but possibly time‐limited, increased risk for malignant lymphomas. There is little to suggest a prominent role for coinherited or common environmental risk factors in malignant lymphomas arising in the context of RA. Instead, lymphomas complicating RA appear to be a direct consequence of the inflammation or its treatment.
The contribution of genotypes at the MEFV and SAA1 loci to amyloidosis and disease severity in patients with familial Mediterranean fever
Authors: Gershoni‐Baruch Ruth , Brik Riva , Zacks Nurit , Shinawi Maruan , Lidar Merav , Livneh Avi 
Published: April 2003

AbstractObjectiveThe clinical profile in familial Mediterranean fever (FMF), including its major manifestation, amyloidosis, is influenced by MEFV allelic heterogeneity and other genetic and/or environmental factors. In this study, we analyzed the contribution of genotypes at the MEFV and SAA1 loci to disease severity and to the development of amyloidosis, and further defined the factors affecting the clinical profile of FMF.MethodsWe investigated a sample of 277 FMF patients (154 men and 123 women), including 62 patients with nephropathic amyloidosis, in whom both FMF alleles had been identified. A detailed chart review, interview, and physical examination were undertaken to determine the patients' demographic characteristics, medical history, clinical manifestations, and treatment. The disease severity score was calculated from the Tel‐Hashomer key. Genotypes at the SAA1 locus (isoforms α, β, and γ) were determined in all patients. The SAA1 13C/T polymorphism of the SAA1 promotor was analyzed in a subset of cases.ResultsThe male:female ratio (154:123, or 1.3) was higher among patients with amyloidosis (40:22, or 1.8) compared with patients without amyloidosis (114:101, or 1.1). Logistic regression analysis showed that homozygosity for the M694V allele (odds ratio [OR] 4.27, 95% confidence interval [95% CI] 2.01–9.07), the presence of the SAAα/α genotype (OR 2.99, 95% CI 1.47–6.09), the occurrence of arthritis attacks (OR 2.43, 95% CI 1.17–5.06), and male sex (OR 1.73, 95% CI 0.90–3.33) were significantly and independently associated with renal amyloidosis. Disease severity was mainly influenced by MEFV mutations and was not associated with genotypes at the SAA1 locus. The SAA1 13T allele was rare, being associated mainly with the SAA γ isoform, and not related to renal amyloidosis.ConclusionOverall, disease severity and the development of amyloidosis in FMF are differentially affected by genetic variations within and outside the MEFV gene.
Ethnic variation in the clinical manifestations of rheumatoid arthritis: Role of HLA–DRB1 alleles
Authors: del Rincón Inmaculada , Battafarano Daniel F. , Arroyo Ramón A. , Murphy Frederick T. , Fischbach Michael , Escalante Agustín 
Published: April 2003

AbstractObjectiveTo assess the extent of ethnic variation in the clinical expression of rheumatoid arthritis (RA) and the role of HLA–DRB1 alleles in this variation.MethodsWe assessed consecutive RA patients for joint findings, subcutaneous nodules, laboratory and radiographic findings, and treatment. We typed HLA–DRB1 alleles to identify those that contain the shared epitope (SE). We adjusted ethnic comparisons for age and sex, and tested for ethnic heterogeneity in the effect of the SE.ResultsWe studied 777 RA patients, 498 of whom were women (64%), 432 were Hispanic (56%), 272 were non‐Hispanic white (NHW; 35%), 53 were African American (AA; 7%), and 20 were Asian (3%). Compared with NHW, Hispanics had significantly more tender joints (17 versus 11), more swollen joints (8 versus 7), more frequent rheumatoid factor (RF) positivity (93% versus 84%), higher erythrocyte sedimentation rate (ESR; 45 versus 36 mm/hr), and a lower number of lifetime disease‐modifying antirheumatic drugs (1.9 versus 2.5). AA were older at onset (46 versus 44 years), had less frequent subcutaneous nodules (18% versus 28%), and higher ESR (42 versus 36 mm/hour) than did NHW. Hispanics and AA were more likely than NHW to be null for the SE (odds ratio [OR] = 4.59 for AA; and OR = 1.61 for Hispanics), and less likely to have 2 SE‐carrying alleles (OR = 0.59 for Hispanics and OR = 0.25 for AA). The number of SE copies was associated with subcutaneous nodules, ESR, RF, and radiographic changes. Ethnic heterogeneity in the effect of the SE was modest.ConclusionsThere is ethnic variation in the clinical expression of RA and in both the frequency and types of SE‐carrying HLA–DRB1 alleles. Some ethnic variation in clinical findings is associated with differences in SE frequency. However, we found that the effect of the SE on the clinical features of RA varies little between ethnic groups.
Health care utilization among older adults with arthritis
Authors: Dunlop Dorothy D. , Manheim Larry M. , Song Jing , Chang Rowland W. 
Published: April 2003

AbstractObjectiveTo evaluate the effect of arthritis on subsequent 2‐year use of health care services and out‐of‐pocket costs among older adults and determine if comorbidities or economic resources mitigate that effect.MethodsData were analyzed from 6,230 participants interviewed in 1993 and 1995 in the Asset and Health Dynamic Survey Among the Oldest Old (AHEAD), a national probability sample of community‐dwelling adults. Baseline arthritis status was ascertained from the report of an arthritis‐related physician's visit or a joint replacement not associated with a hip fracture. The effect of baseline arthritis on the odds of subsequent 2‐year health care utilization and high out‐of‐pocket expenses were estimated from multiple logistic regression controlling for demographic factors, comorbidity, and economic resources.ResultsOlder adults with arthritis are significantly more likely to have a physician visit (odds ratio [OR] 3.0), hospital admission (OR 1.6), outpatient surgery (OR 1.3), receive home health care (OR 1.6), and have out‐of‐pocket cost >$5,000 (OR 1.6) compared with contemporaries having similar demographics (age, sex, racial/ethnic group, marital status), comorbid conditions, and economic resources (education, income, wealth, health insurance), but not reporting arthritis.ConclusionsOlder adults with symptomatic arthritis reported greater medical utilization and cost compared with people not reporting arthritis. These disparities persisted after accounting for differences in demographics, comorbidities, and economic factors. These findings document greater economic burdens on a personal and societal level among people with arthritis. As individuals, older adults with arthritis spend more out‐of‐pocket dollars for health care than their contemporaries without arthritis. On a societal level, these findings of greater health care utilization among people with arthritis point to increasing future demands on the US health care system due to demographic increases in the numbers of older adults with arthritis and support policies aimed at improving arthritis prevention and treatment as well as reducing the economic disparities between those with and without arthritis.
Evaluation of a chiral stationary phase derived from a simple Diels‐Alder reaction
Authors: Thunberg Linda , Allenmark Stig 
Published: April 2003

AbstractThe bicyclic, C2‐symmetric dicarboxylic acid obtained from the cycloaddition of fumaric acid to anthracene can readily be prepared in enantiomerically pure form on a large scale. Conversion of either enantiomer of the diacid into its corresponding bis‐allylamide yields a selector unit, used as a building block in the synthesis of a chiral stationary phase (CSP). The terminal C–C double bonds in the selector unit were used in a hydrosilylation reaction involving a multifunctional hydrosilane to effect polymerization, crosslinking, and immobilization to the vinyl‐silica used as support. A study of the enantiomer‐discriminating abilities of the new CSP was made. Large separation factors were obtained for a series of benzodiazepinones, which were studied in further detail by the use of different retention modifiers. To some extent, rationalization of retention data has been achieved in terms of competition for hydrogen bonding. Chirality 15:400–408, 2003. © 2003 Wiley‐Liss, Inc.
Stereoselective pharmacokinetics of flurbiprofen and formation of covalent adducts with plasma protein in adjuvant‐induced arthritic rats
Authors: Nagao Tomoaki , Tanino Tadatoshi , Iwaki Masahiro 
Published: April 2003

AbstractTo determine the effect of arthritis on the disposition of flurbiprofen (FP) and its acyl glucuronide (FPG) as well as formation of covalent adducts with plasma protein, a pharmacokinetic study was carried out in adjuvant‐induced arthritic (AA) rats. In control animals the pharmacokinetics of FP were stereoselective following intravenous bolus injection of rac‐FP: (–)‐(R)‐FP showed higher plasma clearance (CLtot) and shorter mean residence time (MRT) compared to (+)‐(S)‐FP. The CLtot and clearance for the glucuronide formation (CLglu) of both enantiomers in AA rats were extremely increased compared to those in control rats. Increased total clearance in AA rats was due, at least in part, to a remarkable increase in the plasma unbound fraction of FP, consistent with a decrease in the plasma albumin level. The yield of covalent binding of FP to plasma protein in AA rats was less than that in controls, being consistent with the decrease in the plasma acyl glucuronide level. Chirality 15:423–428, 2003. © 2003 Wiley‐Liss, Inc.
Loss of interneurons innervating pyramidal cell dendrites and axon initial segments in the CA1 region of the hippocampus following pilocarpine‐induced seizures
Authors: Dinocourt Celine , Petanjek Zdravko , Freund Tamas F. , Ben‐Ari Yezekiel , Esclapez Monique 
Published: April 2003

AbstractIn the pilocarpine model of chronic limbic seizures, vulnerability of GABAergic interneurons to excitotoxic damage has been reported in the hippocampal CA1 region. However, little is known about the specific types of interneurons that degenerate in this region. In order to characterize these interneurons, we performed quantitative analyses of the different populations of GABAergic neurons labeled for their peptide or calcium‐binding protein content. Our data demonstrate that the decrease in the number of GAD mRNA‐containing neurons in the stratum oriens of CA1 in pilocarpine‐treated rats involved two subpopulations of GABAergic interneurons: interneurons labeled for somatostatin only (O‐LM and bistratified cells) and interneurons labeled for parvalbumin only (basket and axo‐axonic cells). Stratum oriens interneurons labeled for somatostatin/calbindin or somatostatin/parvalbumin were preserved. The decrease in number of somatostatin‐ and parvalbumin‐containing neurons was observed as early as 72 hours after the sustained seizures induced by pilocarpine injection. Many degenerating cell bodies in the stratum oriens and degenerating axon terminals in the stratum lacunosum‐moleculare were observed at 1 and 2 weeks after injection. In addition, the synaptic coverage of the axon initial segment of CA1 pyramidal cells was significantly decreased in pilocarpine‐treated animals. These results indicate that the loss of somatostatin‐containing neurons corresponds preferentially to the degeneration of interneurons with an axon projecting to stratum lacunosum‐moleculare (O‐LM cells) and suggest that the death of these neurons is mainly responsible for the deficit of dendritic inhibition reported in this region. We demonstrate that the loss of parvalbumin‐containing neurons corresponds to the death of axo‐axonic cells, suggesting that perisomatic inhibition and mechanisms controlling action potential generation are also impaired in this model. J. Comp. Neurol. 459:407–425, 2003. © 2003 Wiley‐Liss, Inc.
Long‐term effects of decreased noradrenergic central nervous system innervation on pain behavior and opioid antinociception
Authors: Jasmin Luc , Boudah Abdennacer , Ohara Peter T. 
Published: April 2003

AbstractHere we examine whether a permanent reduction in the noradrenergic (NA) innervation of the spinal cord leads to a chronic decreased nociceptive threshold. NA denervation of rats was achieved by intrathecal injection of dopamine beta‐hydroxylase antibodies conjugated to the toxin saporin. A subset of animals also underwent unilateral L5 spinal nerve ligature to induce sustained neuropathic pain behavior. NA fibers and terminals were lost throughout the spinal cord 2 weeks after toxin application and were still absent 12 months later, indicating that regeneration did not occur. There was also a widespread loss of NA terminals in the cerebral cortex, whereas innervation of the hypothalamus and amygdala were close to normal and NA innervation of the brainstem was moderately reduced. There was extensive loss of NA cells in the locus coeruleus and A5 and A7 cell groups. Dopaminergic and serotoninergic innervation was normal. Intracerebroventricular injection of the toxin resulted in additional NA reduction in the hypothalamus, amygdala, and A1 and A2 cell groups. Long‐term removal of NA afferents did not affect nociceptive thresholds. Neuropathic animals showed greater mechanical hyperalgesia in the affected hindpaw only during the first 60 days after toxin. Rats lacking NA spinal afferents were less responsive to the antinociceptive effects of morphine, especially in the neuropathic hindpaw, and did not display opioid‐dependent stress analgesia. Finally, in the spinal cord of toxin‐treated rats, immunoreactivity for substance P was decreased, whereas that of its receptor (NK1) was increased. These animals exhibited antinociception to a low dose of an NK1 receptor antagonist. Our results suggest that NA contributes only modestly to determining the nociceptive threshold and that its antinociceptive effects are closely linked to opioidergic and tachykinergic neurotransmission. J. Comp. Neurol. 460:38–55, 2003. © 2003 Wiley‐Liss, Inc.
Anatomical substrates for the central control of sympathetic outflow to interscapular adipose tissue during cold exposure
Authors: Cano Georgina , Passerin Alicia M. , Schiltz Jennifer C. , Card J. Patrick , Morrison Shaun F. , Sved Alan F. 
Published: April 2003

AbstractThe thermogenic activity of interscapular brown adipose tissue (IBAT) in response to physiologic stimuli, such as cold exposure, is controlled by its sympathetic innervation. To determine which brain regions might be involved in the regulation of cold‐evoked increases in sympathetic outflow to IBAT, the present study compared central nervous system (CNS) areas activated by cold exposure with brain regions anatomically linked to the sympathetic innervation of IBAT. Immunocytochemical localization of Fos was examined in the brains of rats exposed to 4°C for 4 hours. In a separate group of rats, the neural circuit involved in IBAT control, including the location of sympathetic preganglionic neurons in the spinal cord, was characterized with pseudorabies virus, a retrograde transynaptic tracer. Central noradrenergic and serotonergic groups related to the sympathetic outflow to IBAT also were identified. Localization of viral antigens at different survival times (66–96 hours) revealed infection in circumscribed CNS populations, but only a subset of the regions comprising this circuitry showed cold‐evoked Fos expression. The raphe pallidus and the ventromedial parvicellular subdivision of the paraventricular hypothalamic nucleus (PVH), both infected at early survival times, were the main areas containing sympathetic premotor neurons activated by cold exposure. Major cold‐sensitive areas projecting to spinal interneurons or to regions containing sympathetic premotor neurons, which became infected at intermediate intervals, included lateral hypothalamic, perifornical, and retrochiasmatic areas, anterior and posterior PVH, ventrolateral periaqueductal gray, and Barrington's nucleus. Areas infected later, most likely related to reception of cold‐related signals, comprised the lateral preoptic area, parastrial nucleus, dorsomedial hypothalamic nucleus, lateral parabrachial nucleus, and nucleus of the solitary tract. These interconnected areas, identified by combining functional and retrograde anatomic approaches, likely constitute the central circuitry responsible for the increase in sympathetic outflow to IBAT during cold‐evoked thermogenesis. J. Comp. Neurol. 460:303–326, 2003. © 2003 Wiley‐Liss, Inc.