bluuebunny/crossref_metadata_2025_split huggingface dataset:
Factors That Impact Symptomatic Diabetic Peripheral Neuropathy in Placebo-Administered Patients From Two 1-Year Clinical Trials
Authors: Tesfaye Solomon , Tandan Rup , Bastyr Edward J. , Kles Keri A. , Skljarevski Vladimir , Price Karen L. ,   for the Ruboxistaurin Study Group
Published: September 2007

OBJECTIVE—The purpose of this study was to evaluate the change in neuropathy symptoms and disease progression in placebo-administered patients from two 1-year studies in which the impact of ruboxistaurin (RBX) in mild diabetic peripheral neuropathy (DPN) was tested.
RESEARCH DESIGN AND METHODS—Data from 262 placebo-administered patients from two identical phase 3, randomized, double-blind trials were combined and analyzed.
RESULTS—After 1 year, change in the neuropathy impairment score of lower limbs [NIS(LL)] (−0.63 points; P = 0.005), vibration detection threshold (VDT) (−0.42 just noticeable difference units; P = 0.003), and Neuropathy Total Symptom Score-6 (NTSS-6) questionnaire (−3.73 points; P &lt; 0.001) improved, whereas some electrophysiology measures and heart rate deep breathing (HRDB) (−0.78 beats; P = 0.003) worsened compared with baseline values. There was a small but significant worsening of A1C (0.28%; P &lt; 0.001), and a greater percentage of patients were using analgesics at the end of the trials (33.6%; P = 0.003). At 1 year, the change in NTSS-6 directly correlated with changes in NIS(LL) and VDT and inversely correlated with the peroneal nerve conduction velocity. On logistic regression analyses, a ≥50% reduction in NTSS-6 score was less likely in patients who used antihypertensive or chronic symptom medication at baseline.
CONCLUSIONS—In placebo-administered patients with mild symptomatic DPN, there was a progressive improvement in symptoms over 12 months, whereas nerve conduction studies and HRDB declined, and clinically significant worsening of DPN would require &gt;1 year of observation.
Corneal Confocal Microscopy Detects Early Nerve Regeneration After Pancreas Transplantation in Patients With Type 1 Diabetes
Authors: Mehra Sanjay , Tavakoli Mitra , Kallinikos Panagiotis A. , Efron Nathan , Boulton Andrew J.M. , Augustine Titus , Malik Rayaz A. 
Published: September 2007

OBJECTIVE—Corneal confocal microscopy (CCM) is a rapid, noninvasive, clinical examination technique that quantifies small nerve fiber pathology. We have used it to assess the neurological benefits of pancreas transplantation in type 1 diabetic patients.
RESEARCH DESIGN AND METHODS—In 20 patients with type 1 diabetes undergoing simultaneous pancreas and kidney transplantation (SPK) and 15 control subjects, corneal sensitivity was evaluated using noncontact corneal esthesiometry, and small nerve fiber morphology was assessed using CCM.
RESULTS—Corneal sensitivity (1.54 ± 0.28 vs. 0.77 ± 0.02, P &lt; 0.0001), nerve fiber density (NFD) (13.8 ± 2.1 vs. 42 ± 3.2, P &lt; 0.0001), nerve branch density (NBD) (4.04 ± 1.5 vs. 26.7 ± 2.5, P &lt; 0.0001), and nerve fiber length (NFL) (2.23 ± 0.2 vs. 9.69 ± 0.7, P &lt; 0.0001) were significantly reduced, and nerve fiber tortuosity (NFT) (15.7 ± 1.02 vs. 19.56 ± 1.34, P = 0.04) was increased in diabetic patients before pancreas transplantation. Six months after SPK, 15 patients underwent a second assessment and showed a significant improvement in NFD (18.04 ± 10.48 vs. 9.25 ± 1.87, P = 0.001) and NFL (3.60 ± 0.33 vs. 1.84 ± 0.33, P = 0.002) with no change in NBD (1.38 ± 0.74 vs. 1.38 ± 1.00, P = 1.0), NFT (15.58 ± 1.20 vs. 16.30 ± 1.19, P = 0.67), or corneal sensitivity (1.23 ± 0.39 vs. 1.54 ± 00.42, P = 0.59).
CONCLUSIONS—Despite marked nerve fiber damage in type 1 diabetic patients undergoing pancreas transplantation, small fiber repair can be detected within 6 months of pancreas transplantation using CCM. CCM is a novel noninvasive clinical technique to assess the benefits of therapeutic intervention in human diabetic neuropathy.
Reduced Incidence of Lower-Limb Amputations in the Diabetic Population of a German City, 1990–2005
Authors: Trautner Christoph , Haastert Burkhard , Mauckner Peter , Gätcke Lena-Maria , Giani Guido 
Published: September 2007

OBJECTIVE—We evaluated whether the incidence of amputations in one German city (Leverkusen, population ∼160,000) had decreased between 1990 and 2005.
RESEARCH DESIGN AND METHODS—From all three hospitals in the city, we obtained complete lists of nontraumatic lower-limb amputations in 1990–1991 and 1994–2005. Only the first observed amputation in residents of Leverkusen was counted. A total of 692 patients met the inclusion criteria. Data about the population stucture, separately for each year of the observation period, were received from the city administration and the Federal Office of Statistics. To test for time trend, we fitted Poisson regression models.
RESULTS—Of all subjects, 72% had known diabetes and 58% were male. Mean age was 71.7 years. Incidence rates in the diabetic population (standardized to the estimated German diabetic population per 100,000 person-years) varied considerably between years (maximum 549 in 1990, minimum 281 in 2004). In the diabetic population, the estimated relative risk (RR) per year was 0.976 (95% CI 0.958–0.996, P = 0.0164). The same trend was observed when only amputations above the ankle (n = 352) (RR 0.970 [95% CI 0.943–0.997], P = 0.0318) were considered. Over 15 years, an estimated reduction of amputations above the toe level by 37.1% (95% CI 12.3–54.8) results. There was no significant change of incident amputations in the nondiabetic population (RR 1.022 [0.989–1.056], P = 0.1981).
CONCLUSIONS—This finding is likely to be due to improved management of the diabetic foot syndrome after a network of specialized physicians and defined clinical pathways for wound treatment and metabolic control were introduced.
Lymphocyte Subsets in the Nasal Mucosa and Peripheral Blood during Experimental Rhinovirus Infection
Authors: Winther Birgit , Innes Donald J. , Bratsch John , Hayden Frederick G. 
Published: September 2007

The local cellular response during rhinovirus infection was studied with immunohistochemical staining of lymphocyte subpopulations in the lamina propria of the nasal mucosa (inferior turbinate) in 25 biopsies from volunteers with experimental rhinovirus colds and compared with biopsies from healthy volunteers. Biopsies from rhinovirus infected volunteers, taken either in the early phase of the infection (days 3 and 5) or during convalescence (day 14) were evaluated in a semiquantitative fashion for degree of infiltration. Lymphocyte subpopulations also were counted on coded specimens. During experimental rhinovirus infection, no change could be observed in the overall degree of lymphocytic infiltration or in the numbers of T and B lymphocytes compared with control specimens. The overall degree of lymphocyte infiltration in the nasal mucosa was mild to moderate and consisted principally of T lymphocytes and only a few scattered B lymphocytes. Few natural killer lymphocytes were seen. These findings are similar to those in normal nasal mucosa and in contrast to the findings after topical application of recombinant interferon, which often results in a heavy lymphocyte infiltration. Lymphocyte subpopulation in the peripheral blood did not change when compared with prechallenge values in nine rhinovirus-infected volunteers.
Endoscopic Septal Spur Resection
Authors: Lanza Donald C. , Rosin Deborah Farb , Kennedy David W. 
Published: September 2007

A variety of surgical approaches exists for the management of nasal septal spurs in patients who undergo endoscopic sinus surgery (ESS). Treatment of septal spurs in the past has been frequently addressed by septoplasty which can result in increased bleeding and length of surgical procedure as well as mandate postoperative nasal packing. Individually each of these problems can jeopardize the success of endoscopic sinus surgery. An endoscopic approach, which targets the septal spur alone, can minimize perioperative morbidity. The purpose of this paper is to demonstrate the effectiveness of endoscopic septal spur resection (ESSR) for the management of significant septal spurs in 8 patients who underwent concurrent ESSR during ESS for chronic sinusitis. Surgical technique and postoperative results are discussed and suggest that ESSR is a valuable alternative to more traditional techniques.
Rh‐TPPTS intercalated layered double hydroxides as hydroformylation catalyst
Authors: Wei Min , Zhang Xian , Evans David G. , Duan Xue , Li Xianjun , Chen Hua 
Published: September 2007

AbstractTrans‐RhCl(CO)(TPPTS)2 [TPPTS, trisodium salt of tri‐(m‐sulfophenyl)‐phosphine] and TPPTS ligands have been cointercalated into zinc–aluminum‐layered double hydroxides (ZnAl‐LDHs) by in situ complexation, and the catalytic performances of the resulting materials for 1‐hexene hydroformylation have been investigated. The intercalated materials were characterized by means of XRD, FTIR, ICP, and 31P MAS NMR. The rhodium complex and TPPTS ligands coexist in the interlayer galleries of LDH (denoted as RhP2‐P‐ZnnAl‐LDH, where n denotes as the molar ratio Zn/Al), with an interlayer spacing of ca. 1.58 nm. Compared with the catalytic properties of the corresponding water‐oil biphasic catalyst under similar reaction conditions, RhP2‐P‐Zn3Al‐LDH showed better reusability and activity. Furthermore, compared with a related material prepared by ion exchange, the RhP2‐P‐Zn3Al‐LDH showed better activity and selectivity towards aldehyde. The influence of the Zn/Al molar ratio in RhP2‐P‐ZnnAl‐LDH has also been studied, and it was found that higher selectivity to aldehydes and lower activity were obtained with increasing Zn/Al molar ratio. © 2007 American Institute of Chemical Engineers AIChE J, 2007
Modeling of coat‐hanger die under vibrational extrusion
Authors: Qu Jin‐Ping , Zhang Xiao‐Ming 
Published: September 2007

AbstractThe distributions of the pulsatile pressure field, the pulsatile velocity field, and the pulsatile resident time of the polymeric melt in the coat‐hanger die are derived by using the pulsation of volumetric flow rate and pressure. Subsequently, formulae of the manifold radius and the slope of the manifold are deduced via volumetric flow rate pulsation. Polypropylene (PP) was employed for the experiments of the vibrational extrusion. The results indicate that the average extrusion pressure declines with frequency or amplitude decreasing; the distribution of residence time along the width of the coat‐hanger die performs uniformly during the vibrational extrusion process; the theoretical extrusion pressure well agrees with the experimental pressure; the experiments of tensile test, impact test implicate that vibration improves the mechanical properties of products; differential scanning calorimetry testing demonstrates that the melting point of PP is moved to a higher temperature value, and the endothermic enthalpy and the crystallinity are improved as well when superimposing the vibrational force field. Accordingly, the model of the coat‐hanger die under vibrational extrusion is well consistent with the experiments. © 2007 Wiley Periodicals, Inc. J Appl Polym Sci, 2008
Characterization of discriminant human brain antigenic targets in neuropsychiatric systemic lupus erythematosus using an immunoproteomic approach
Authors: Lefranc Didier , Launay David , Dubucquoi Sylvain , Seze Jérôme De , Dussart Patricia , Vermersch Marie , Hachulla Eric , Hatron Pierre‐Yves , Vermersch Patrick , Mouthon Luc , Prin Lionel 
Published: September 2007

AbstractObjectiveTo characterize discriminant human brain antigenic targets in patients with neuropsychiatric systemic lupus erythematosus (NPSLE), using a standardized immunoproteomic approach.MethodsSelf‐IgG reactivity against normal and injured human brain tissues was studied by Western blotting of sera from 169 subjects, 16 patients with NPSLE, 12 patients with SLE without neuropsychiatric manifestations (non‐NPSLE), 32 patients with Sjögren's syndrome with or without central nervous involvement, 82 patients with multiple sclerosis, and 27 healthy subjects. A proteomic approach was then applied to characterize discriminant antigens identified after comparisons of all patterns.ResultsThe serum self‐IgG reactivity patterns against human brain tissue differed significantly between patients with NPSLE and the control groups. Four normal brain antigenic bands were specifically or preferentially recognized by sera from NPSLE patients (p240, p90, p77, and p24). Protein band p240 was characterized as microtubule‐associated protein 2B (MAP‐2B), p77 as Hsp70–71, and p24 as triosephosphate isomerase. Protein band p90 was not characterized. In contrast, 1 other protein band (p56, characterized as septin 7) was never recognized by sera from NPSLE patients but was recognized by a majority of sera from non‐NPSLE patients.ConclusionOur findings show that the immunoproteomic approach is a reliable method for assessing serum self‐IgG reactivities against human brain tissue in NPSLE. Our characterization of some of the identified discriminant antigens, such as MAP‐2B, triosephosphate isomerase, and septin 7, suggests that the stability of neuronal microtubules might be involved in the pathophysiology of NPSLE.
T cells expressing allograft inflammatory factor 1 display increased chemotaxis and induce a profibrotic phenotype in normal fibroblasts in vitro
Authors: Galdo Francesco Del , Jiménez Sergio A. 
Published: September 2007

AbstractObjectiveAllograft inflammatory factor 1 (AIF‐1) was first identified in rat cardiac allografts undergoing chronic rejection. The vasculopathy of chronic allograft rejection is strikingly similar to that seen in patients with systemic sclerosis (SSc). We previously demonstrated AIF‐1 expression in inflammatory cells infiltrating skin and lungs from SSc patients, but its role in SSc pathogenesis is unknown. The present study was undertaken to investigate the effects of AIF‐1 on T cell migration and production of cytokines capable of modulating normal dermal fibroblast functions.MethodsStably transfected Jurkat T cells expressing 2 AIF‐1 splicing variants were prepared, and their migration toward fibroblast monolayers assayed in Transwell cultures. Cytokine production was assessed by real‐time polymerase chain reaction (PCR) and multiplex enzyme‐linked immunosorbent assay. Fibroblast gene expression was quantified by real‐time PCR, and collagen production by Western blot analysis of culture media.ResultsAIF‐1 significantly increased Jurkat T cell migration toward fibroblast monolayers. Expression of AIF‐1 isoform 2 in Jurkat T cells up‐regulated their production of interleukin‐4 (IL‐4) and IL‐17. Conditioned media from AIF‐1–expressing clones stimulated synthesis of types I and III collagen and expression of IL‐6, transforming growth factor β, endothelin receptor, and α‐smooth muscle actin by normal dermal fibroblasts.ConclusionThese results suggest that AIF‐1 may participate in the early pathogenesis of SSc by promoting tissue T cell infiltration and production of cytokines capable of inducing the expression of a fibrotic phenotype in normal fibroblasts.
Cutaneous changes of nephrogenic systemic fibrosis: Predictor of early mortality and association with gadolinium exposure
Authors: Todd Derrick J. , Kagan Anna , Chibnik Lori B. , Kay Jonathan 
Published: September 2007

AbstractObjectiveNephrogenic systemic fibrosis (NSF) is a rapidly progressive, debilitating condition that causes cutaneous and visceral fibrosis in patients with renal failure. Little is known about its prevalence or etiology. The aim of this study was to establish the prevalence of NSF and associated risk factorsMethodsTwo cohorts of patients were recruited from 6 outpatient hemodialysis centers and examined for cutaneous changes of NSF, which were defined using a scoring system based on hyperpigmentation, hardening, and tethering of skin on the extremities. Demographic data were gathered, mortality was followed up prospectively for 24 months, and gadolinium exposure was ascertained for a subgroup of patients in the second cohort.ResultsExamination reproducibility was 97% in cohort 1. In cohort 2, 25 (13%) of 186 patients demonstrated cutaneous changes of NSF. Twenty‐four–month mortality following examination was 48% and 20% in patients with and those without cutaneous changes of NSF, respectively (adjusted hazard ratio 2.9, 95% confidence interval [95% CI] 1.4–5.9). Cutaneous changes of NSF were observed in 16 (30%) of 54 patients with prior exposure to gadopentetate dimeglumine contrast during imaging studies. Exposure to gadolinium‐containing contrast was associated with an increased risk of developing cutaneous changes of NSF (odds ratio 14.7, 95% CI 1.9–117.0) compared with nonexposed patients.ConclusionIn patients receiving hemodialysis, NSF is an underrecognized disorder that is associated with increased mortality. Exposure to gadolinium‐containing contrast material appears to be a significant risk factor for the development of NSF.
CXCR5‐ and CCR7‐dependent lymphoid neogenesis in a murine model of chronic antigen‐induced arthritis
Authors: Wengner Antje M. , Höpken Uta E. , Petrow Peter K. , Hartmann Sven , Schurigt Uta , Bräuer Rolf , Lipp Martin 
Published: September 2007

AbstractObjectiveRheumatoid arthritis (RA) is a chronic inflammatory autoimmune disease with unknown etiology and only partially defined pathogenesis. The aim of this study was to establish a murine model of chronic arthritis in which the development of tertiary lymphoid tissue, a hallmark of human RA, is locally induced, and to characterize the roles of the homeostatic chemokine receptors CXCR5 and CCR7 in this process.MethodsWe developed a modified model of chronic antigen‐induced arthritis (AIA) in mice with a strong bias toward inflammation. Disease pathology was assessed up to 9 months in wild‐type, CXCR5‐deficient, and CCR7‐deficient mice by determination of knee joint swelling and cellular and humoral immune responses, as well as by histologic analysis of arthritic knee joints.ResultsIn this novel model of AIA, mice developed organized ectopic lymphoid follicles with topologically segregated B cell and T cell areas, high endothelial venules, and germinal center formation within the chronically inflamed synovial tissue. Analysis of the initiation and progression of AIA in wild‐type, CXCR5−/−, and CCR7−/− mice revealed a reduction of acute inflammatory parameters in both knockout strains as well as significantly reduced joint destruction in CXCR5−/− mice. Most importantly, the development and organization of tertiary lymphoid tissue were significantly impaired in CXCR5‐deficient and CCR7‐deficient mice.ConclusionOur results suggest that an inflammatory microenvironment efficiently triggers lymphoid neogenesis in autoimmune diseases such as RA. Moreover, the generation of autoreactive tertiary lymphoid tissues, which is entirely dependent on homeostatic chemokines, may in turn maintain local aberrant chronic immune responses.
Severe fibrosis and increased expression of fibrogenic cytokines in the gastric wall of systemic sclerosis patients
Authors: Manetti Mirko , Neumann Elena , Milia Anna Franca , Tarner Ingo H. , Bechi Paolo , Matucci‐Cerinic Marco , Ibba‐Manneschi Lidia , Müller‐Ladner Ulf 
Published: September 2007

AbstractObjectiveSystemic sclerosis (SSc) is a connective tissue disorder characterized by fibrosis of the skin and internal organs. Although the esophagus is the most frequently affected part of the gastrointestinal tract, all other segments can be involved. The present study was undertaken to evaluate the fibrotic process and the expression of fibrogenic cytokines in the gastric wall of SSc patients with gastroesophageal involvement.MethodsFull‐thickness surgical and endoscopic gastric biopsy samples were obtained from 14 SSc patients and 10 controls. Tissue sections were either stained with Masson's trichrome or by immunohistochemistry and analyzed for the expression of types I, III, and IV collagen, α‐smooth muscle actin (α‐SMA), transforming growth factor β (TGFβ), connective tissue growth factor (CTGF), and endothelin 1 (ET‐1).ResultsIn the gastric wall of SSc patients, Masson's trichrome staining and immunohistochemistry for types I and III collagen revealed a high amount of collagen in the lamina propria that increased toward the muscularis mucosae. In addition, muscle layers showed features of atrophy, with wide areas of focal fibrosis surrounding smooth muscle cells. Type IV collagen was present around glands and small vessels, suggesting a thickening of the basal lamina. The expression of the fibrogenic cytokines TGFβ and CTGF, ET‐1, and the myofibroblast marker α‐SMA was stronger in SSc patients than in controls.ConclusionA pronounced deposition of collagen, the presence of myofibroblasts, and increased expression of several profibrotic factors are important hallmarks in the stomach of patients with SSc. The fibrotic involvement of the gastric wall may account for muscle atrophy leading to stomach hypomotility in SSc.
Prevention of cartilage destruction with intraarticular osteoclastogenesis inhibitory factor/osteoprotegerin in a murine model of osteoarthritis
Authors: Shimizu Sadanori , Asou Yoshinori , Itoh Soichiro , Chung Ung‐Il , Kawaguchi Hiroshi , Shinomiya Kenichi , Muneta Takeshi 
Published: September 2007

AbstractObjectiveTo investigate the effect of osteoclastogenesis inhibitory factor/osteoprotegerin (OPG) on chondrocytes in the development of osteoarthritis (OA) in vivo.MethodsTo determine the role of endogenous OPG in the progression of OA, OA was surgically induced in OPG+/− mice and their wild‐type (WT) littermates. To determine the role of exogenous OPG, knee joints of C57BL/6J mice with surgically induced OA were injected intraarticularly with recombinant human OPG (rHuOPG) or vehicle 5 times a week. All mice were euthanized 4 weeks after OA induction; joints were harvested and evaluated immunohistochemically.ResultsAlthough OA changes were induced in both WT and OPG+/− mice, the degenerative changes in the articular cartilage were significantly enhanced in OPG+/− mice. In C57BL/6J mice with surgically induced OA, intraarticular OPG administration protected the articular cartilage from the progression of OA. The Mankin and cartilage destruction scores in OPG‐treated animals were ∼50% of those seen in the control group. Furthermore, OPG administration significantly protected articular cartilage thickness. Findings of the TUNEL assay indicated that rHuOPG prevented chondrocyte apoptosis in joints with surgically induced OA. Results of immunostaining indicated that OPG protein was detected in the synovium and in resident chondrocytes at higher levels in the OPG‐treated group than in the control group.ConclusionThese data indicate that endogenous OPG had a protective effect against the cartilage destruction that occurs during OA progression. Furthermore, direct administration of rHuOPG to articular chondrocytes prevented cartilage destruction in an experimental murine model of OA via prevention of chondrocyte apoptosis.