bluuebunny/crossref_metadata_2025_split huggingface dataset:
Intraperitoneal Pressure and Intra-Abdominal Pressure: Are they the Same?
Authors: Al-Hwiesh Abdullah , Al-Mueilo Sameer , Saeed Ibrahiem , Al-Muhanna Fahd A. 
Published: March 2011

Background In peritoneal dialysis (PD), a standard therapy for patients with end-stage renal disease (ESRD), the effects of using the peritoneum as an exchange membrane and of dialysate dwelling within the peritoneal cavity creates some mechanical changes, including an increase in intraperitoneal pressure (IPP) that might lead to intra-abdominal hypertension (IAH) and abdominal compartment syndrome (ACS). The diagnosis of IAH and ACS depend on intra-abdominal measurement of IAP by an indirect technique. There is no clear distinction between IPP and intra-abdominal pressure (IAP). Our objective in this study was to find if there is real difference between IPP and IAP. Methods This study was conducted at the PD unit of King Fahd Hospital of the University, Al-Khobar, between July 2008 and January 2009. To be included, patients had to have known ESRD for at least 5 years, to be 18 years of age or older at enrollment, with stable body weight and blood pressure, and with no clinical signs of overhydration. Patients with congestive heart failure III and IV (New York Heart Association criteria) and severe pulmonary disease, psychiatric illnesses, neurogenic bladder, known history of peritonitis, or medical or surgical abdominal intervention in the preceding 3 months were excluded. We measured IAP by the direct technique through the peritoneal catheter and by an indirect technique using an intravesical catheter. Results The 25 patients who met the inclusion criteria included 13 men and 12 women, with a mean age of 53 ± 2 years (range: 18 – 76 years). The predominant causes of ESRD were diabetes mellitus and glomerulonephritis. Mean IPP in the dry state (supine) was 9.49 ± 5 mmHg, and mean IAP was 9.4 ± 5.4 mmHg ( p = 0.9). In the dry state (erect), the mean IPP increased to 16.9 ± 7.2 mmHg, and the mean IAP, to 16.4 ± 6.9 mmHg ( p = 0.8). In the filled state (supine), mean IPP was 12.6 ± 4.7 mmHg, and mean IAP, 12.8 ± 4.8 mmHg ( p = 0.88); the erect pressures were 21.4 ± 7 mmHg and 21.6 ± 6.9 mmHg respectively ( p = 0.9). Conclusions Our findings indicate that there is no statistical difference between IPP and IAP in either the erect or the supine position.
Atorvastatin Reduces High Glucose Toxicity in Rat Peritoneal Mesothelial Cells
Authors: Carrión Blanca , Pérez–Martínez Francisco C. , Monteagudo Silvia , Pérez–Carrión María D. , Gómez–Roldán Carmen , Ceña Valentín , Pérez–Martínez Juan 
Published: March 2011

Objective Continuous exposure of the peritoneal membrane to high glucose dialysis solutions can produce functional alterations in this membrane. We studied the toxic effects of high glucose (50 mmol/L and 83 mmol/L) and its reversal by atorvastatin (0.5 – 5 μmol/L) on cultures of rat peritoneal mesothelial cells (PMCs). Methods Rat PMCs were harvested from the peritonea of male Sprague–Dawley rats and grown in M199 medium supplemented with 10% fetal bovine serum. The effects of high glucose (50 mmol/L and 83 mmol/L) on levels of reactive oxygen species (ROS), on caspase 3 activity, and on phospho-p38 mitogen-activated protein kinase (MAPK) in the cultures were evaluated. Results Exposure to high glucose (for 4, 8, and 24 hours) increased intracellular levels of ROS and phospho-p38 MAPK (indices of cellular toxicity). Atorvastatin blocked these toxic effects of high glucose, being more effective against 50 mmol/L glucose (protective effects were observed above 0.5 μmol/L) than against 83 mmol/L (protective effects were observed above 2.5 μmol/L). Atorvastatin was also able to prevent glucose-induced increase in caspase 3 activity. Conclusions The present study shows that high glucose may promote oxidative stress and may activate apoptotic pathways in rat PMCs. These toxic effects could be reversed by atorvastatin.
Rapid Improvement in the Signs and Symptoms of Rheumatoid Arthritis Following Certolizumab Pegol Treatment Predicts Better Longterm Outcomes: Post-hoc Analysis of a Randomized Controlled Trial
Authors: KEYSTONE EDWARD C. , CURTIS JEFFREY R. , FLEISCHMANN ROY M. , FURST DANIEL E. , KHANNA DINESH , SMOLEN JOSEF S. , MEASE PHILIP J. , SCHIFF MICHAEL H. , COTEUR GEOFFROY , DAVIES OWEN , COMBE BERNARD 
Published: March 2011

Objective.To assess the kinetics of response to certolizumab pegol (CZP), and association between rapid response and longterm outcomes, in patients with active rheumatoid arthritis (RA).Methods.This was a post-hoc analysis of the randomized, double-blind RAPID 1 study in patients who received methotrexate (MTX) and either CZP 200 mg subcutaneously or placebo every 2 weeks for 52 weeks. Clinical and radiographic outcomes at Week 52 were evaluated based on the Disease Activity Score 28 (DAS28) ≥ 1.2 and American College of Rheumatology 20% (ACR20) responses at Week 6 and Week 12.Results.Clinical responses [European League Against Rheumatism (EULAR), DAS28 ≥ 1.2, and ACR20 responses] were rapid in CZP-treated patients. Week 12 DAS28 ≥ 1.2 responders had better clinical and radiographic outcomes at Week 52 compared with nonresponders. Among Week 12 responders, incremental benefit of earlier response was observed: Week 6 DAS28 ≥ 1.2 responders and ACR20 responders had significantly higher ACR response rates and were more likely to achieve remission at Week 52 than Week 12 responders. Patients with a clinical response at Week 6 had faster, more meaningful sustained improvements in patient-derived outcomes than those responding by Week 12 only.Conclusion.Rapid attainment of clinical response in patients with RA is associated with improved longterm outcomes. Analysis of the kinetics of response to CZP during the first 12 weeks of therapy potentially permits informed prediction of clinical success or need to alter treatment. In patients not achieving a clinical response at Week 12 treatment adjustment should be considered. Trial registration NCT00152386.
Respiratory Dysfunction in Patients With Sepsis: Protective Effect of Diabetes Mellitus
Authors: Yang Yong , Salam Zakir-Hussain Abdul , Ong Biauw Chi , Yang Kok Soong 
Published: March 2011

Background
Sepsis is a common complication in patients with diabetes mellitus. In a Western population, risk of respiratory dysfunction was lower in diabetic patients with sepsis.

Objective
To compare organ dysfunction, particularly respiratory dysfunction, between sepsis patients with and without diabetes mellitus in an Asian population.

Method
Hospital discharge data were collected for the period 2004 through 2008. Patients with sepsis, diabetes mellitus, and organ dysfunction were identified by using the International Statistical Classification of Diseases and Related Health Problems, 9th Revision, Australian Modification codes.

Results
Of the 383 238 patients hospitalized during the 5 years, 2943 of the 9221 who had sepsis also had diabetes (31.9%).The most common organ dysfunctions in patients with sepsis were renal (31.5%), cardiovascular (19.2%), and respiratory (10.9%). Among patients with sepsis, respiratory dysfunction was less likely in patients with diabetes (9.4%) than in those without (11.6%; P = .002), but renal dysfunction was more likely in patients with diabetes (46.5%) than in those without (24.4%; P &lt; .001). However, only 27.6% of patients with diabetes had a respiratory source of sepsis compared with 33.4% in patients without diabetes (P &lt; .001). Among patients with sepsis, diabetes mellitus was a significant and independent predictor of respiratory dysfunction (odds ratio, 0.80; 95% confidence interval, 0.66–0.98) after adjustments for age, sex, ethnicity, admission to intensive care, number of comorbid conditions, and other infection sources.

Conclusion
Among an Asian population, respiratory dysfunction in patients with sepsis is less likely to develop in those with diabetes than in those without diabetes.
Hypoxia-Inducible Factor-1α–Dependent Protection from Intestinal Ischemia/Reperfusion Injury Involves Ecto-5′-Nucleotidase (CD73) and the A2B Adenosine Receptor
Authors: Hart Melanie L. , Grenz Almut , Gorzolla Iris C. , Schittenhelm Jens , Dalton Julee H. , Eltzschig Holger K. 
Published: March 2011

Abstract
Intestinal ischemia/reperfusion injury (IR) is characterized by intermittent loss of perfusion to the gut, resulting in dramatic increases in morbidity and mortality. Based on previous studies indicating an anti-inflammatory role for hypoxia-inducible factor (HIF)-1–elicited enhancement of extracellular adenosine production via ecto-5′-nucleotidase (CD73) and signaling through the A2B adenosine receptor (A2BAR), we targeted HIF-1 during IR using pharmacological or genetic approaches. Initial studies with pharmacological HIF activation indicated attenuation of intestinal injury with dimethyloxallyl glycine (DMOG) treatment during murine IR. Although DMOG treatment was associated with induction of CD73 transcript and protein, DMOG protection was abolished in cd73−/− mice. Similarly, DMOG treatment enhanced A2BAR transcript and protein levels, whereas DMOG protection was abolished in A2BAR−/− mice. Finally, studies of mice with conditional HIF-1α deletion in intestinal epithelia or pharmacological inhibition of HIF-1 with 17-(dimethylaminoethylamino)-17-demethoxygeldanamycin revealed enhanced tissue injury during IR. These studies indicated a tissue-protective role of HIF-dependent enhancement of intestinal adenosine generation and signaling during intestinal IR.
Histone Deacetylase Inhibitor LAQ824 Augments Inflammatory Responses in Macrophages through Transcriptional Regulation of IL-10
Authors: Wang Hongwei , Cheng Fengdong , Woan Karrune , Sahakian Eva , Merino Oscar , Rock-Klotz Jennifer , Vicente-Suarez Ildefonso , Pinilla-Ibarz Javier , Wright Kenneth L. , Seto Edward , Bhalla Kapil , Villagra Alejandro , Sotomayor Eduardo M. 
Published: March 2011

Abstract
APCs are important in the initiation of productive Ag-specific T cell responses and the induction of T cell anergy. The inflammatory status of the APC at the time of encounter with Ag-specific T cells plays a central role in determining such divergent T cell outcomes. A better understanding of the regulation of proinflammatory and anti-inflammatory genes in its natural setting, the chromatin substrate, might provide novel insights to overcome anergic mechanisms mediated by APCs. In this study, we show for the first time, to our knowledge, that treatment of BALB/c murine macrophages with the histone deacetylase inhibitor LAQ824 induces chromatin changes at the level of the IL-10 gene promoter that lead to enhanced recruitment of the transcriptional repressors HDAC11 and PU.1. Such an effect is associated with diminished IL-10 production and induction of inflammatory cells able of priming naive Ag-specific T cells, but more importantly, capable of restoring the responsiveness of anergized Ag-specific CD4+ T cells.
Cross Talk between Glucocorticoid and Estrogen Receptors Occurs at a Subset of Proinflammatory Genes
Authors: Cvoro Aleksandra , Yuan Chaoshen , Paruthiyil Sreenivasan , Miller Oliver H. , Yamamoto Keith R. , Leitman Dale C. 
Published: March 2011

Abstract
Glucocorticoids exert potent anti-inflammatory effects by repressing proinflammatory genes. We previously demonstrated that estrogens repress numerous proinflammatory genes in U2OS cells. The objective of this study was to determine if cross talk occurs between the glucocorticoid receptor (GR) and estrogen receptor (ER)α. The effects of dexamethasone (Dex) and estradiol on 23 proinflammatory genes were examined in human U2OS cells stably transfected with ERα or GR. Three classes of genes were regulated by ERα and/or GR. Thirteen genes were repressed by both estradiol and Dex (ER/GR-repressed genes). Five genes were repressed by ER (ER-only repressed genes), and another five genes were repressed by GR (GR-only repressed genes). To examine if cross talk occurs between ER and GR at ER/GR-repressed genes, U2OS-GR cells were infected with an adenovirus that expresses ERα. The ER antagonist, ICI 182780 (ICI), blocked Dex repression of ER/GR-repressed genes. ICI did not have any effect on the GR-only repressed genes or genes activated by Dex. These results demonstrate that ICI acts on subset of proinflammatory genes in the presence of ERα but not on GR-activated genes. ICI recruited ERα to the IL-8 promoter but did not prevent Dex recruitment of GR. ICI antagonized Dex repression of the TNF response element by blocking the recruitment of nuclear coactivator 2. These findings indicate that the ICI–ERα complex blocks Dex-mediated repression by interfering with nuclear coactivator 2 recruitment to GR. Our results suggest that it might be possible to exploit ER and GR cross talk for glucocorticoid therapies using drugs that interact with ERs.
HIV-1 Tat-Mediated Induction of Platelet-Derived Growth Factor in Astrocytes: Role of Early Growth Response Gene 1
Authors: Bethel-Brown Crystal , Yao Honghong , Callen Shannon , Lee Young Han , Dash Prasanta K. , Kumar Anil , Buch Shilpa 
Published: March 2011

Abstract
HIV-associated neurologic disorders (HAND) are estimated to affect almost 60% of HIV-infected individuals. HIV encephalitis, the pathologic correlate of the most severe form of HAND, is often characterized by glial activation, cytokine-chemokine dysregulation, and neuronal damage and loss. However, the severity of HIV encephalitis correlates better with glial activation rather than viral load. Using the macaque model, it has been demonstrated that SIV encephalitis correlates with increased expression of the mitogen platelet-derived growth factor (PDGF) B chain in the brain. The goal of this study was to explore the role of PDGF-B chain in HIV-associated activation and proliferation of astrocytes. Specifically, the data demonstrate that exposure of rat and human astrocytes to the HIV-1 protein Tat resulted in the induction of PDGF at both the mRNA and protein levels. Furthermore, PDGF-BB induction was regulated by activation of ERK1/2 and JNK signaling pathways and the downstream transcription factor early growth response 1. Chromatin immunoprecipitation assays demonstrated binding of Egr-1 to the PDGF-B promoter. Exposure of astrocytes to PDGF-BB in turn led to increased proliferation and the release of proinflammatory cytokines MCP-1 and IL-1β. Because astrogliosis is linked to disease severity, understanding its regulation by PDGF-BB could aid in the development of therapeutic intervention strategies for HAND.
Plasticity of Human Regulatory T Cells in Healthy Subjects and Patients with Type 1 Diabetes
Authors: McClymont Stephanie A. , Putnam Amy L. , Lee Michael R. , Esensten Jonathan H. , Liu Weihong , Hulme Maigan A. , Hoffmüller Ulrich , Baron Udo , Olek Sven , Bluestone Jeffrey A. , Brusko Todd M. 
Published: March 2011

Abstract
Regulatory T cells (Tregs) constitute an attractive therapeutic target given their essential role in controlling autoimmunity. However, recent animal studies provide evidence for functional heterogeneity and lineage plasticity within the Treg compartment. To understand better the plasticity of human Tregs in the context of type 1 diabetes, we characterized an IFN-γ–competent subset of human CD4+CD127lo/−CD25+ Tregs. We measured the frequency of Tregs in the peripheral blood of patients with type 1 diabetes by epigenetic analysis of the Treg-specific demethylated region (TSDR) and the frequency of the IFN-γ+ subset by flow cytometry. Purified IFN-γ+ Tregs were assessed for suppressive function, degree of TSDR demethylation, and expression of Treg lineage markers FOXP3 and Helios. The frequency of Tregs in peripheral blood was comparable but the FOXP3+IFN-γ+ fraction was significantly increased in patients with type 1 diabetes compared to healthy controls. Purified IFN-γ+ Tregs expressed FOXP3 and possessed suppressive activity but lacked Helios expression and were predominately methylated at the TSDR, characteristics of an adaptive Treg. Naive Tregs were capable of upregulating expression of Th1-associated T-bet, CXCR3, and IFN-γ in response to IL-12. Notably, naive, thymic-derived natural Tregs also demonstrated the capacity for Th1 differentiation without concomitant loss of Helios expression or TSDR demethylation.
Differential B7–CD28 Costimulatory Requirements for Stable and Inflationary Mouse Cytomegalovirus-Specific Memory CD8 T Cell Populations
Authors: Arens Ramon , Loewendorf Andrea , Redeker Anke , Sierro Sophie , Boon Louis , Klenerman Paul , Benedict Chris A. , Schoenberger Stephen P. 
Published: March 2011

Abstract
CMV establishes a lifelong persistent infection, and viral immune-modulating strategies are important in facilitating this. A particularly diverse CD8 T cell response develops as a result of this host-virus détente, with the CMV-specific memory T cell pool displaying unique functions and phenotypes. To gain insight into the factors that regulate CMV-specific CD8 T cell responses, we examined the influence of the B7–CD28 costimulatory pathway on magnitude, kinetics, and phenotype. Initial expansion of mouse CMV-specific CD8 T cells that establish stable memory pools was severely lower in mice lacking B7–CD28 signaling, and the resulting memory levels also remained reduced during persistent/latent infection. In contrast, expansion of CD8 T cells that undergo memory inflation during chronic infection was less affected in the absence of B7–CD28 costimulatory signals, eventually reaching the levels seen in wild-type mice at later times. Regardless of their differential requirements for B7–CD28 signals, both stable and inflationary memory T cell populations showed normal cytotoxic capacity. These results reveal that B7–CD28 costimulation differentially regulates the magnitude and kinetics of the multifaceted CD8 T cell response that develops during CMV infection.
IL-27 and IL-21 Are Associated with T Cell IL-10 Responses in Human Visceral Leishmaniasis
Authors: Ansari Nasim Akhtar , Kumar Rajiv , Gautam Shalini , Nylén Susanne , Singh Om Prakash , Sundar Shyam , Sacks David 
Published: March 2011

Abstract
IL-10 is believed to underlie many of the immunologic defects in human visceral leishmaniasis (VL). We have identified CD4+CD25−Foxp3− T cells as the major source of IL-10 in the VL spleen. IL-27, a member of the IL-6/IL-12 cytokine family, has been shown to promote development of IL-10–producing T cells, in part by upregulating their production of autocrine IL-21. We investigated whether IL-27 and IL-21 are associated with human VL. IL-27 was elevated in VL plasma, and at pretreatment, spleen cells showed significantly elevated mRNA levels of both IL-27 subunits, IL-27p28 and EBI-3, as well as IL-21, compared with posttreatment biopsies. CD14+ spleen cells were the main source of IL-27 mRNA, whereas CD3+ T cells were the main source of IL-21. IL-27 mRNA could be strongly upregulated in normal donor macrophages with IFN-γ and IL-1β, conditions consistent with those in the VL spleen. Last, a whole-blood assay revealed that most VL patients could produce Ag-specific IFN-γ and IL-10 and that the IL-10 could be augmented with recombinant human IL-21. Thus, proinflammatory cytokines acting on macrophages in the VL spleen have the potential to upregulate IL-27, which in turn can induce IL-21 to expand IL-10–producing T cells as a mechanism of feedback control.
Cutting Edge: Attrition of Plasmodium-Specific Memory CD8 T Cells Results in Decreased Protection That Is Rescued by Booster Immunization
Authors: Schmidt Nathan W. , Harty John T. 
Published: March 2011

Abstract
Sterile protection against infection with Plasmodium sporozoites requires high numbers of memory CD8 T cells. However, infections with unrelated pathogens, as may occur in areas endemic to malaria, can dramatically decrease pre-existing memory CD8 T cells. It remains unknown whether unrelated infections will compromise numbers of Plasmodium-specific memory CD8 T cells and thus limit the duration of antimalarial immunity generated by subunit vaccination. We show that P. berghei circumsporozoite-specific memory CD8 T cells underwent significant attrition in numbers in mice subjected to unrelated infections. Attrition was associated with preferential loss of effector memory CD8 T cells and reduced immunity to P. berghei sporozoite challenge. However, and of relevance to deployment of Plasmodium vaccines in areas endemic to malaria, attrition of memory CD8 T cells was reversed by booster immunization, which restored protection. These data suggest that regular booster immunizations may be required to sustain protective vaccine-induced Plasmodium-specific memory CD8 T cells in the face of attrition caused by unrelated infections.
Serum N-Terminal Propeptide of Collagen Type I is Associated with the Number of Bone Metastases in Breast and Prostate Cancer and Correlates to Other Bone Related Markers
Authors: Leeming D.J. , Koizumi M. , Qvist P. , Barkholt V. , Zhang C. , Henriksen K. , Byrjalsen I. , Karsdal M.A. 
Published: March 2011

BackgroundA number of biomarkers have been proven potentially useful for their ability to indicate bone metastases (BM) in cancer patients. The aim of this study was to investigate the relative utility of a newly developed N-terminal propeptide of collagen type I (PINP) human serum assay for the detection of BM in cancer patients. This assay has a corresponding rat PINP assay which in the future might help in translational science between rodent and human trials.MethodsParticipants were 161 prostate, lung and breast cancer patients stratified by number of BM(Soloway score). PINP was assessed and correlated to number of BM. Additionally, the PINP marker was correlated to bone resorption of young (ALPHA CTX-I)- and aged bone (BETA CTX-I); number of osteoclasts (Tartrate-resistant acid phosphatase 5b, TRACP5B) and osteoclast activity (CTX-I/TRACP5B).ResultsPINP was significantly elevated in breast- and prostate cancer patients +BM, compared to –BM ( P < 0.001), however not in lung cancer patients. A strong linear association was seen between PINP and the number of BMs. Significant elevation of PINP was observed at Soloway scores 1–4 (<0 BM) compared with score 0 (0 BM) ( P < 0.001). The correlation between bone resorption of young bone or aged bone and bone formation was highly significant in patients +BM and –BM ( P < 0.0001).ConclusionsData suggest that the present PINP potentially could determine skeletal involvement in patients with breast or prostate cancer. Correlations suggested that coupling between bone resorption and bone formation was maintained in breast- and prostate cancer patients.
Edematous Erythema at the Hands and Feet Probably Caused by the Traditional Herb “Radix Astragali”
Authors: Kogure Toshiaki , Tatsumi Takeshi , Oku Yuko 
Published: March 2011

Objective To describe a patient with erhythema and edema after Radix Astragali was added to a kampo formula. Case summary A 21-year-old male, who was diagnosed as having atopic dermatitis in 1989, demonstrated systemic dry eruptions and consulted our department for treatment with traditional herbal medicine (THM) in 2004. The oral administration of herbal medicine resulted in decreased symptoms as well as a reduction in the serum IgE level. In August 2007, he complained of sweating on the neck and we added Radix Astragali to the previous formula. About 18 hours after he ingested the new formula including Radix Astragali, erhythema appeared with swelling of the bilateral hands and feet. Administration of the formula was discontinued and about 48 hours later, his symptoms had almost disappeared. Astragaloside, which is the main ingredient of Radix Astragali, was negative on lymphocyte transforming test (LTT) and we could not determine the ingredient that induced erhythema. Conclusion We consider that the Radix Astragali induced acute erhythema with swelling based on the clinical course. Acute edematous erythema due to THM is very rare and we discuss allergic reactions to traditional herbs and review the litrature.