bluuebunny/crossref_metadata_2025_split huggingface dataset:
Retraction Notice: An Outlook on Ovarian Cancer and Borderline Ovarian Tumors: Focus on Genomic and Proteomic Findings
Authors: Tinelli Andrea , Vergara Daniele , Martignago Roberta , Leo Giuseppe , Pisanò Maurizio , Malvasi Antonio 
Published: June 2009

The above article is a plagiarized version of another article entitled “Ovarian Cancer Biomarkers: A Focus on Genomic and Proteomic Findings, 2007 Aug; 8(5): 335–342” written by the same authors and published in “Current Genomics”. Bentham Science apologizes to the readers of the journal for not detecting this omission during the publishing process.

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Regeneration of the Pancreas in Adult Zebrafish
Authors: Moss Jennifer B. , Koustubhan Punita , Greenman Melanie , Parsons Michael J. , Walter Ingrid , Moss Larry G. 
Published: June 2009

OBJECTIVE
Regenerating organs in diverse biological systems have provided clues to processes that can be harnessed to repair damaged tissue. Adult mammalian β-cells have a limited capacity to regenerate, resulting in diabetes and lifelong reliance on insulin. Zebrafish have been used as a model for the regeneration of many organs. We demonstrate the regeneration of adult zebrafish pancreatic β-cells. This nonmammalian model can be used to define pathways for islet-cell regeneration in humans.

RESEARCH DESIGN AND METHODS
Adult transgenic zebrafish were injected with a single high dose of streptozotocin or metronidazole and anesthetized at 3, 7, or 14 days or pancreatectomized. Blood glucose measurements were determined and gut sections were analyzed using specific endocrine, exocrine, and duct cell markers as well as markers for dividing cells.

RESULTS
Zebrafish recovered rapidly without the need for insulin injections, and normoglycemia was attained within 2 weeks. Although few proliferating cells were present in vehicles, ablation caused islet destruction and a striking increase of proliferating cells, some of which were Pdx1 positive. Dividing cells were primarily associated with affected islets and ducts but, with the exception of surgical partial pancreatectomy, were not extensively β-cells.

CONCLUSIONS
The ability of the zebrafish to regenerate a functional pancreas using chemical, genetic, and surgical approaches enabled us to identify patterns of cell proliferation in islets and ducts. Further study of the origin and contribution of proliferating cells in reestablishing islet function could provide strategies for treating human diseases.
Endoplasmic Reticulum Stress Regulates Adipocyte Resistin Expression
Authors: Lefterova Martina I. , Mullican Shannon E. , Tomaru Takuya , Qatanani Mohammed , Schupp Michael , Lazar Mitchell A. 
Published: June 2009

OBJECTIVE
Resistin is a secreted polypeptide that impairs glucose metabolism and, in rodents, is derived exclusively from adipocytes. In murine obesity, resistin circulates at elevated levels but its gene expression in adipose tissue is paradoxically reduced. The mechanism behind the downregulation of resistin mRNA is poorly understood. We investigated whether endoplasmic reticulum (ER) stress, which is characteristic of obese adipose tissue, regulates resistin expression in cultured mouse adipocytes.

RESEARCH DESIGN AND METHODS
The effects of endoplasmic stress inducers on resistin mRNA and secreted protein levels were examined in differentiated 3T3-L1 adipocytes, focusing on the expression and genomic binding of transcriptional regulators of resistin. The association between downregulated resistin mRNA and induction of ER stress was also investigated in the adipose tissue of mice fed a high-fat diet.

RESULTS
ER stress reduced resistin mRNA in 3T3-L1 adipocytes in a time- and dose-dependent manner. The effects of ER stress were transcriptional because of downregulation of CAAT/enhancer binding protein-α and peroxisome proliferator–activated receptor-γ transcriptional activators and upregulation of the transcriptional repressor CAAT/enhancer binding protein homologous protein-10 (CHOP10). Resistin protein was also substantially downregulated, showing a close correspondence with mRNA levels in 3T3-L1 adipocytes as well as in the fat pads of obese mice.

CONCLUSIONS
ER stress is a potent regulator of resistin, suggesting that ER stress may underlie the local downregulation of resistin mRNA and protein in fat in murine obesity. The paradoxical increase in plasma may be because of various systemic abnormalities associated with obesity and insulin resistance.
Adult Stature and Diabetes Complications in Patients With Type 1 Diabetes
Authors: Wadén Johan , Forsblom Carol , Thorn Lena M. , Saraheimo Markku , Rosengård-Bärlund Milla , Heikkilä Outi , Hietala Kustaa , Ong Ken , Wareham Nicholas , Groop Per-Henrik 
Published: June 2009

OBJECTIVE
Short adult stature has previously been associated with cardiovascular disease, but its relationship with the microvascular complications of diabetes is uncertain. Therefore, we evaluated the association between adult stature and prevalence and incidence of diabetic microvascular complications.

RESEARCH DESIGN AND METHODS
This cross-sectional and longitudinal study comprises 3,968 adult patients with type 1 diabetes from the Finnish Diabetic Nephropathy (FinnDiane) Study and 1,246 adult patients from the Diabetes Control and Complications Trial (DCCT). In FinnDiane, diabetic nephropathy was defined as urinary albumin excretion ≥300 mg/24 h, dialysis, or renal transplantation. Retinopathy was divided into background and proliferative (laser-treated) retinopathy. In the DCCT, original nephropathy (class 1–6) and retinopathy (Early Treatment of Diabetic Retinopathy Study) classifications were used.

RESULTS
In the FinnDiane study, patients in the lowest quartile of adult height had increased risks of prevalent diabetic nephropathy (odds ratio [OR] 1.71, 95% CI 1.44–2.02) and prevalent laser-treated retinopathy (1.66, 1.43–1.93) compared with other patients. Similarly, in the DCCT, patients in the lowest quartile of adult height had increased risks of incident diabetic nephropathy class 4–6 (hazard ratio 2.70, 95% CI 1.59–4.59) and incident proliferative retinopathy (2.06, 1.15–3.71). In the FinnDiane study, the associations were largely explained by childhood exposure to diabetes. However, in the DCCT, where a greater proportion of patients had diabetes onset &gt;18 years, the association with nephropathy was independent of childhood diabetes exposure.

CONCLUSIONS
Short adult stature is associated with microvascular complications in patients with type 1 diabetes. These findings are compatible with either childhood diabetes exposure or “common soil” or both as potential explanations.
Kir6.2 Variant E23K Increases ATP-Sensitive K+ Channel Activity and Is Associated With Impaired Insulin Release and Enhanced Insulin Sensitivity in Adults With Normal Glucose Tolerance
Authors: Villareal Dennis T. , Koster Joseph C. , Robertson Heather , Akrouh Alejandro , Miyake Kazuaki , Bell Graeme I. , Patterson Bruce W. , Nichols Colin G. , Polonsky Kenneth S. 
Published: June 2009

OBJECTIVE
The E23K variant in the Kir6.2 subunit of the ATP-sensitive K+ channel (KATP channel) is associated with increased risk of type 2 diabetes. The present study was undertaken to increase our understanding of the mechanisms responsible. To avoid confounding effects of hyperglycemia, insulin secretion and action were studied in subjects with the variant who had normal glucose tolerance.

RESEARCH DESIGN AND METHODS
Nine subjects with the E23K genotype K/K and nine matched subjects with the E/E genotype underwent 5-h oral glucose tolerance tests (OGTTs), graded glucose infusion, and hyperinsulinemic-euglycemic clamp with stable-isotope–labeled tracer infusions to assess insulin secretion, action, and clearance. A total of 461 volunteers consecutively genotyped for the E23K variant also underwent OGTTs. Functional studies of the wild-type and E23K variant potassium channels were conducted.

RESULTS
Insulin secretory responses to oral and intravenous glucose were reduced by ∼40% in glucose-tolerant subjects homozygous for E23K. Normal glucose tolerance with reduced insulin secretion suggests a change in insulin sensitivity. The hyperinsulinemic-euglycemic clamp revealed that hepatic insulin sensitivity is ∼40% greater in subjects with the E23K variant, and these subjects demonstrate increased insulin sensitivity after oral glucose. The reconstituted E23K channels confirm reduced sensitivity to inhibitory ATP and increase in open probability, a direct molecular explanation for reduced insulin secretion.

CONCLUSIONS
The E23K variant leads to overactivity of the KATP channel, resulting in reduced insulin secretion. Initially, insulin sensitivity is enhanced, thereby maintaining normal glucose tolerance. Presumably, over time, as insulin secretion falls further or insulin resistance develops, glucose levels rise resulting in type 2 diabetes.
Validation of a Belt Model for Prediction of Hub Forces from a Rolling Tire
Authors: Lecomte C. , Graham W. R. , O’Boy D. J. 
Published: June 2009

Abstract
An integrated model is under development which will be able to predict the interior noise due to the vibrations of a rolling tire structurally transmitted to the hub of a vehicle. Here, the tire belt model used as part of this prediction method is first briefly presented and discussed, and it is then compared to other models available in the literature. This component will be linked to the tread blocks through normal and tangential forces and to the sidewalls through impedance boundary conditions. The tire belt is modeled as an orthotropic cylindrical ring of negligible thickness with rotational effects, internal pressure, and prestresses included. The associated equations of motion are derived by a variational approach and are investigated for both unforced and forced motions. The model supports extensional and bending waves, which are believed to be the important features to correctly predict the hub forces in the midfrequency (50–500 Hz) range of interest. The predicted waves and forced responses of a benchmark structure are compared to the predictions of several alternative analytical models: two three dimensional models that can support multiple isotropic layers, one of these models include curvature and the other one is flat; a one-dimensional beam model which does not consider axial variations; and several shell models. Finally, the effects of internal pressure, prestress, curvature, and tire rotation on free waves are discussed.
Proximal Tibia Reconstruction With a Porous Tantalum Cone in a Patient With Charcot Arthropathy
Authors: Troyer Joshua , Levine Brett R. 
Published: June 2009

Neuropathic arthritis, or Charcot arthropathy, is a rapidly destructive process associated with nerve damage and periarticular insensitivity. Most commonly it is associated with diabetes mellitus, tabes dorsalis, syringomyelia, or other peripheral nerve disorders. Clinical manifestations of this disorder classically include gross deformity, crepitus, lack of proprioception, joint effusion, calor, and decreased awareness of pain in the affected joint. Often the clinical picture is difficult to distinguish from septic arthritis. Radiographic findings are typically worse than portrayed during clinical examination. Rapid destruction of the articular surface with bony fragmentation is commonly found. The incidence of neuropathic arthritis among all diabetic patients is relatively small, ranging between 0.15% and 0.4%.
Historically, there have been conflicting reports as to the efficacy of total knee arthroplasty (TKA) in patients with neuropathic arthritis. However, recent literature on the use of modern implants has been more optimistic as to the success of TKA. Difficulties associated with severe bone loss, poor bone quality, and ligamentous laxity may necessitate the use of structural allografts/augments, as well as stemmed and/or constrained TKA components. This article presents a case of a patient with Charcot arthropathy of the knee secondary to diabetes mellitus (type 2) treated successfully with a minimally constrained TKA and a porous tantalum cone (Zimmer, Warsaw, Indiana) as an “internal plate,” for reconstruction of a combined segmental/cavitary defect of the proximal tibia. At 2-year follow-up, radiographs revealed stable TKA components with reconstitution of the fragmented proximal tibia around an osseointegrated porous cone.
Bread Mold Osteomyelitis in the Femur
Authors: Wilkins Ross M. , Hahn David B. , Blum Raymond 
Published: June 2009

Rhizopus osteomyelitis is an uncommon and often fatal infection that usually occurs in immunocompromised patients. The infection is commonly referred to as “bread mold.” The usual course of treatment is Amphotericin B, debridement, and, if needed, amputation of the affected limb. This article details a rare case of postoperative Rhizopus osteomyelitis in an otherwise healthy patient.
The patient originally presented at another institution for anterior cruciate ligament repair after a ski injury. Postoperatively, he developed clinical evidence of infection. He was referred to our institution with stiffness and swelling in the knee as well as weight loss and decreased range of motion. Fluid collection was visible on magnetic resonance imaging. Arthroscentesis was cultured for fungus and bacteria, and the fungal cultures were positive for Rhizopus species. An attempt at limb salvage was made. Debridement, use of a cement spacer loaded with Amphotericin B, systemic antifungal therapy, and 23 hyperbaric oxygen treatments were used to eradicate the disease. Four surgeries were needed to eradicate the disease, and 10 months after initial presentation, the patient had a distal femoral endoprosthesis placed in his leg. Laboratory tests returned to normal and frozen sections were negative for fungus. At 3-year follow-up, the patient reported a musculoskeletal functional score of 50% and had no evidence of recurrent infection.
Involvement of CD252 (CD134L) and IL-2 in the Expression of Cytotoxic Proteins in Bacterial- or Viral-Activated Human T Cells
Authors: Walch Michael , Rampini Silvana K. , Stoeckli Isabelle , Latinovic-Golic Sonja , Dumrese Claudia , Sundstrom Hanna , Vogetseder Alexander , Marino Joseph , Glauser Daniel L. , van den Broek Maries , Sander Peter , Groscurth Peter , Ziegler Urs 
Published: June 2009

Abstract
Regulation of cytotoxic effector molecule expression in human CTLs after viral or bacterial activation is poorly understood. By using human autologous dendritic cells (DCs) to prime T lymphocytes, we found perforin only highly up-regulated in virus- (HSV-1, vaccinia virus) but not in intracellular bacteria- (Listeria innocua, Listeria monocytogenes, Mycobacterium tuberculosis, Chlamydophila pneumoniae) activated CTLs. In contrast, larger quantities of IFN-γ and TNF-α were produced in Listeria-stimulated cultures. Granzyme B and granulysin were similarly up-regulated by all tested viruses and intracellular bacteria. DCs infected with HSV-1 showed enhanced surface expression of the costimulatory molecule CD252 (CD134L) compared with Listeria-infected DC and induced enhanced secretion of IL-2. Adding blocking CD134 or neutralizing IL-2 Abs during T cell activation reduced the HSV-dependent up-regulation of perforin. These data indicate a distinct CTL effector function in response to intracellular pathogens triggered via differing endogenous IL-2 production upon costimulation through CD252.
Myeloperoxidase Deficiency Attenuates Lipopolysaccharide-Induced Acute Lung Inflammation and Subsequent Cytokine and Chemokine Production
Authors: Haegens Astrid , Heeringa Peter , van Suylen Robert Jan , Steele Chad , Aratani Yasuaki , O'Donoghue Robert J. J. , Mutsaers Steven E. , Mossman Brooke T. , Wouters Emiel F. M. , Vernooy Juanita H. J. 
Published: June 2009

Abstract
Lung neutrophilia is common to a variety of lung diseases. The production of reactive oxygen and nitrogen species during neutrophil oxidative burst has been associated with protein and DNA damage. Myeloperoxidase (MPO) is an enzyme stored in the azurophilic granula of neutrophils. It is important in host defense because it generates the reactive oxidant hypochlorous acid and has been described to play a role in the activation of neutrophils during extravasation. We hypothesized that MPO contributes directly to the development of acute lung neutrophilia via stimulation of neutrophil extravasation and indirectly to the subsequent production of cytokines and chemokines in the lung. To test this hypothesis, wild-type (WT) and Mpo−/− mice were given a single LPS instillation, after which the development of neutrophil-dominated lung inflammation, oxidative stress, and cytokine and chemokine levels were examined. Mpo−/− mice demonstrated a decreased lung neutrophilia that peaked earlier than neutrophilia in WT mice, which can be explained by decreased neutrophil chemoattractant levels in LPS-exposed Mpo−/− compared with WT mice. However, oxidative stress levels were not different in LPS-exposed WT and Mpo−/− mice. Furthermore, in vivo findings were confirmed by in vitro studies, using isolated neutrophils. These results indicate that MPO promotes the development of lung neutrophilia and indirectly influences subsequent chemokine and cytokine production by other cell types in the lung.
Neutrophil-Derived IL-6 Limits Alveolar Barrier Disruption in Experimental Ventilator-Induced Lung Injury
Authors: Wolters Paul J. , Wray Charlie , Sutherland Rachel E. , Kim Sophia S. , Koff Jon , Mao Ying , Frank James A. 
Published: June 2009

Abstract
IL-6 is a biological marker of ventilator-associated lung injury that may contribute to alveolar barrier dysfunction in acute respiratory distress syndrome. To determine whether IL-6 affects alveolar barrier disruption in a model of ventilator-induced lung injury, we examined alveolar barrier albumin flux in wild-type (WT) mice given an IL-6-blocking Ab (IL6AB) and mice deficient in IL-6 (IL6KO). Albumin flux was significantly higher in mice given IL6AB compared with mice given a control Ab. Unexpectedly, albumin flux was similar in WT and IL6KO mice. To examine the mechanisms for these findings, lung neutrophil accumulation (myeloperoxidase activity) was compared, revealing a correlation between lung neutrophil accumulation and albumin flux. IL6AB mice had significantly more lung neutrophils than WT and IL6KO mice, which were similar. Therefore, to determine whether the cellular source of IL-6 influences neutrophil accumulation and alveolar barrier function, chimeric mice were compared. WT/KO chimeras (WT mice with IL6KO hematopoietic cells) showed significantly greater albumin flux and neutrophil accumulation with mechanical ventilation than WT/WT mice. Neutrophil depletion decreased albumin flux in WT and WT/KO mice. IL6KO neutrophils were more adherent in an in vitro assay compared with WT neutrophils. IL-6 from a hematopoietic cell source limits alveolar barrier disruption potentially by reducing neutrophil contact with the endothelium. Modulation of IL-6 signaling in a cell type-specific fashion may be a therapeutic target for patients with acute lung injury.
Tuberculosis Subunit Vaccination Provides Long-Term Protective Immunity Characterized by Multifunctional CD4 Memory T Cells
Authors: Lindenstrøm Thomas , Agger Else Marie , Korsholm Karen S. , Darrah Patricia A. , Aagaard Claus , Seder Robert A. , Rosenkrands Ida , Andersen Peter 
Published: June 2009

Abstract
Improved vaccines capable of promoting long-term cellular immunity are urgently required for a number of diseases that remain global health problems. In the present study, we demonstrate that a tuberculosis subunit vaccine, Ag85B-ESAT-6/CAF01 (where ESAT-6 is early secreted antigenic target of 6 kDa and CAF01 is cationic adjuvant formulation 01), induces very robust memory CD4 T cell responses that are maintained at high levels for &gt;1 year postvaccination. This long-term, vaccine-induced memory response protects against a challenge with Mycobacterium tuberculosis at levels that are comparable to or better than those of bacillus Calmette-Guérin. Characterization of the CD4 memory T cells by multicolor flow cytometry demonstrated that the long-lived memory population consisted almost exclusively of TNF-α+IL-2+ and IFN-γ+TNF-α+IL-2+ multifunctional T cells. In addition, memory cells isolated &gt;1 year postvaccination maintained a strong, vaccine-specific proliferative potential. Long-term memory induced by the BCG vaccine contained fewer multifunctional T cells and was biased toward effector cells mainly of the TNF-α+IFN-γ+-coexpressing subset. Ag85B-ESAT-6/CAF01 vaccination very efficiently sustained multifunctional CD4 T cells that accumulated at the site of infection after M. tuberculosis challenge, whereas the response in unvaccinated animals was characterized by CD4 effector T cells. Our data demonstrate that adjuvanted subunit vaccines can promote long-term protective immune responses characterized by high levels of persisting multifunctional T cells and that the quality and profile of this response is sustained postinfection.
Fc Receptor-Like 3 Protein Expressed on IL-2 Nonresponsive Subset of Human Regulatory T Cells
Authors: Nagata Satoshi , Ise Tomoko , Pastan Ira 
Published: June 2009

Abstract
Fc receptor-like 3 (FCRL3) is a cell surface protein homologous to Fc receptors. The FCRL3 gene is present in humans but not in mice. We found that FCRL3 protein is expressed on 40% of human naturally occurring CD4+ regulatory T (nTreg) cells (CD4+CD25+CD127low). Sorted nTreg cells with the surface phenotype FCRL3+ and FCRL3− were both hypoproliferative to TCR stimulation and both suppressive on proliferation of conventional T cells (CD4+CD25−) in vitro. They both expressed forkhead box p3 (Foxp3) protein, the intracellular regulatory T cell marker. However, in contrast to FCRL3− nTreg cells, FCRL3+ nTreg cells were not stimulated to proliferate by the addition of exogenous IL-2. In addition, Foxp3+ cells induced from conventional T cells by TGF-β treatment did not exhibit FCRL3 expression. These results suggest that the FCRL3+ subset of human nTreg cells identified in this study arise in vivo and Foxp3 expression alone is not sufficient to induce FCRL3 expression. FCRL3 may be involved in human-specific mechanisms to control the generation of nTreg cells.