bluuebunny/crossref_metadata_2025_split huggingface dataset:
Increasing work-place healthiness with the probiotic Lactobacillus reuteri: A randomised, double-blind placebo-controlled study
Authors: Tubelius Py , Stan Vlaicu , Zachrisson Anders 
Published: November 2005

Abstract

Background
Short term illnesses, usually caused by respiratory or gastrointestinal diseases are disruptive to productivity and there is relatively little focus on preventative measures. This study examined the effect of the probiotic Lactobacillus reuteri protectis (ATCC55730) on its ability to improve work-place healthiness by reducing short term sick-leave caused by respiratory or gastrointestinal infections.

Methods
262 employees at TetraPak in Sweden (day-workers and three-shift-workers) that were healthy at study start were randomised in a double-blind fashion to receive either a daily dose of 108 Colony Forming Units of L. reuteri or placebo for 80 days. The study products were administered with a drinking straw. 181 subjects complied with the study protocol, 94 were randomised to receive L. reuteri and 87 received placebo.

Results
In the placebo group 26.4% reported sick-leave for the defined causes during the study as compared with 10.6% in the L. reuteri group (p < 0.01). The frequency of sick-days was 0.9% in the placebo group and 0.4% in the L. reuteri group (p < 0.01). Among the 53 shift-workers, 33% in the placebo group reported sick during the study period as compared with none in the L. reuteri group(p < 0.005).
Increased PAI-1 plasma levels and risk of death from dengue: no association with the 4G/5G promoter polymorphism
Authors: Mairuhu ATA , Setiati TE , Koraka P , Hack CE , Leyte A , Faradz SMH , ten Cate H , Brandjes DPM , Osterhaus ADME , Reitsma PH , van Gorp ECM 
Published: November 2005

Abstract

Background
Dengue virus infected patients have high plasminogen activator inhibitor type I (PAI-1) plasma concentrations. Whether the insertion/deletion (4G/5G) polymorphism in the promotor region of the PAI-1 gene is associated with increased PAI-1 plasma concentrations and with death from dengue is unknown. We, therefore, investigated the relationship between the 4G/5G polymorphism and PAI-1 plasma concentrations in dengue patients and risk of death from dengue.

Methods
A total of 194 patients admitted to the Dr. Kariadi Hospital in Semarang, Indonesia, with clinical suspected severe dengue virus infection were enrolled. Blood samples were obtained on day of admission, days 1, 2 and 7 after admission and at a 1-month follow-up visit. Plasma concentrations of PAI-1 were measured using a sandwich ELISA kit. The PAI-1 4G/5G polymorphism was typed by allele-specific PCR analysis.

Results
Concentrations of PAI-1 on admission and peak values of PAI-1 during admission were higher than the values measured in healthy controls. Survival was significantly worse in patients with PAI-1 concentrations in the highest tertile (at admission: OR 4.7 [95% CI 0.9–23.8], peak value during admission: OR 6.3 [95%CI 1.3–30.8]). No association was found between the PAI-1 4G/5G polymorphism, and PAI-1 plasma concentrations, dengue disease severity and mortality from dengue.

Conclusion
These data suggest that the 4G/5G polymorphism has no significant influence on PAI-1 concentrations in dengue virus infected patients and is not associated with the risk of death from dengue. Other factors contributing to the variability of PAI-1 plasma concentrations in patients with dengue need to be explored.
Effects of co-administered dexamethasone and diclofenac potassium on pain, swelling and trismus following third molar surgery
Authors: Bamgbose Babatunde Olamide , Akinwande Jelili Adisa , Adeyemo Wasiu Lanre , Ladeinde Akinola Ladipo , Arotiba Godwin Toyin , Ogunlewe Mobolanle Olugbemiga 
Published: November 2005

Abstract

Background
The apparent interactions between the mechanisms of action of non-steroidal anti-inflammatory drugs (NSAIDS) and steroids suggest that co-therapy may provide beneficial inflammatory and pain relief in the absence of side effects. The aim of the study was to compare the effect of co-administered dexamethasone and diclofenac potassium (diclofenac K) with diclofenac K alone on the postoperative pain, swelling and trismus after surgical removal of third molars.

Patients and Methods
A prospective randomized double-blind study was conducted at the Department of Oral and Maxillofacial Surgery, Lagos University Teaching Hospital, Nigeria. A total of 100 patients were randomly allocated to two treatment groups of dexamethasone (prophylactic 8 mg and postoperative 4 mg IV) and diclofenac K (50 mg Oral before and after surgery), and diclofenac K alone (as with first group). The overall analgesic efficacy of the drug combinations was assessed postoperatively by determination of pain intensity using a category rating scale. Facial swelling was measured using a tape measure placed from tragus to gonion to tragus, while interincisal mouth-opening of patients was measured using a vernier calibrated caliper pre-operatively and post-operatively.

Results
Co-administration of dexamethasone and diclofenac K was significantly superior to diclofenac alone for the relief of pain (P < 0.05), and facial swelling up to post-operative 48 hour (P < 0.05). However, there was no significant difference for trismus relief between the two medication protocols (P > 0.05).

Conclusion
This study illustrates enhanced effects of co-administered dexamethasone and diclofenac K on short-term post-operative pain and swelling, compared to diclofenac potassium alone in third molar surgery.
Cationic liposomes induce apoptosis through p38 MAP kinase–caspase-8–Bid pathway in macrophage-like RAW264.7 cells
Authors: Iwaoka Sayaka , Nakamura Tomoko , Takano Shuhei , Tsuchiya Seishi , Aramaki Yukihiko 
Published: November 2005

Abstract
We have demonstrated that cationic liposomes composed of stearylamine (SA-liposomes) induce apoptosis in a variety of cells, but the mechanism responsible for the cellular death is not clear. In this paper, we investigated the signaling pathways implicated in SA-liposome-induced apoptosis in the macrophage-like cell line RAW264.7. Treatment with SA-liposomes caused the activation of mitogen-activated proein kinases (MAPKs), especially p38 and c-jun N-terminal kinase, and apoptosis was only inhibited upon the addition of a specific inhibitor for p38. N-acetylcysteine, a scavenger of reactive oxygen species (ROS), effectively inhibited the activation of p38 and cellular death, indicating that the activation induced by ROS is an initial step in the process of apoptosis triggered by SA-liposomes. Caspase-8 was activated by p38, and caspase-8-dependent cleavage of Bid was also observed. No down-regulation of bcl-2 expression, and no cleavage of Bax protein were observed. Taken together, our results suggest that apoptosis of RAW264.7 by SA-liposomes was mediated by the MAPK p38 and a caspase-8-dependent Bid-cleavage pathway. Moreover, we found that ROS can contribute intimately to the SA-liposome-induced cell death in RAW264.7.
Prostaglandin E2 promotes degranulation-independent release of MCP-1 from mast cells
Authors: Nakayama Takayuki , Mutsuga Noriko , Yao Lei , Tosato Giovanna 
Published: November 2005

Abstract
Mast cells (MCs) are common components of inflammatory infiltrates and a source of proangiogenic factors. Inflammation is often accompanied by vascular changes. However, little is known about modulation of MC-derived proangiogenic factors during inflammation. In this study, we evaluated the effects of the proinflammatory mediator prostaglandin E2 (PGE2) on MC expression and release of proangiogenic factors. We report that PGE2 dose-dependentlyinduces primary MCs to release the proangiogenic chemokine monocyte chemoattractant protein-1 (MCP-1). This release of MCP-1 is complete by 2 h after PGE2 exposure, reaches levels of MCP-1 at least 15-fold higher than background, and is not accompanied by degranulation or increased MCP-1 gene expression. By immunoelectron microscopy, MCP-1 is detected within MCs at a cytoplasmic location distinct from the secretory granules. Dexamethasone and cyclosporine A inhibit PGE2-induced MCP-1 secretion by ∼60%. Agonists of PGE2 receptor subtypes revealed that the EP1 and EP3 receptors can independently mediate MCP-1 release from MCs. These observations identify PGE2-induced MCP-1 release from MCs as a pathway underlying inflammation-associated angiogenesis and extend current understanding of the activities of PGE2.
Bovine natural killer cells acquire cytotoxic/effector activity following activation with IL-12/15 and reduce Mycobacterium bovis BCG in infected macrophages
Authors: Endsley Janice J , Endsley Mark A , Estes D Mark 
Published: November 2005

Abstract
Bovine natural killer (NK) cells were recently identified by positive selection of a NK cell-activating receptor p46 (NKp46)+ CD3– lymphocyte population, which expresses CD25 and CD8 and lyses tumor cell lines following stimulation with recombinant interleukin-2. In the current work, we characterize the cytotoxic/effector potential of a CD3–CD8–CD11b– population isolated through negative selection of bovine peripheral blood leukocytes. This population is CD25loCD62hi when isolated and becomes CD25hiCD62Llo following cytokine stimulation. Activated bovine NK cells increase expression of granulysin, interferon-γ, and perforin and have cytotoxic activity against human tumor cells and Mycobacterium bovis bacillus Calmette-Guerin-infected alveolar and monocyte-derived macrophages. Expression of a bovine homologue of the CD56 neural adhesion molecule expressed by human NK cells was detected in mRNA from brain tissue but was not detected in peripheral blood mononuclear cells or purified NK cell mRNA. Analysis of mRNA from nonstimulated peripheral blood NK cells demonstrates the constitutive expression of homologues of human NK receptors NKp46, CD244, and CD94 and the granule proteins granulysin and perforin. Phorbol ester-stimulated CD8+ T cells also expressed CD244 and CD94, and CD4+ T cells expressed CD94. These NK cell receptors bearing T lymphocytes may represent memory subsets characterized in humans. The results of these studies demonstrate that bovine NK cells may play an important role in the innate immune responses of cattle.
Virulent clinical isolates of Mycobacterium tuberculosis grow rapidly and induce cellular necrosis but minimal apoptosis in murine macrophages
Authors: Park Jae Seuk , Tamayo Marcela Henao , Gonzalez-Juarrero Mercedes , Orme Ian M , Ordway Diane J 
Published: November 2005

Abstract
In this study, we investigated the ability of four clinical isolates of Mycobacterium tuberculosis representing a range of virulence for their capacity to grow in bone marrow-derived macrophages. The rate of growth of each of the isolates in macrophages reflected their known virulence, but the most virulent isolates strongly induced production of the cytokine tumor necrosis factor α. A key difference, however, was the degree of cell cytotoxicity observed with the more virulent strains ater several days in culture. Staining of cell monolayers for DNA fragmentation indicative of apoptosis showed that this was minimal and only evident to any degree in macrophages infected with the most virulent strains. In contrast, electron microscopy revealed damage of macrophages consistent with cell necrosis. These results suggest that rapid intracellular growth rate and induction of necrotic cell death within host macrophages are virulence factors of M. tuberculosis in the early stages of bacterial infection. They further imply that infected cell apoptosis, regarded as a defense mechanism or cross-priming mechanism, plays a minimal role.
Chemical inhibitors of TNF signal transduction in human neutrophils point to distinct steps in cell activation
Authors: Han Hyunsil , Roberts Julia , Lou Olivia , Muller Willam A , Nathan Noah , Nathan Carl 
Published: November 2005

Abstract
Chemical screening identified three small compounds that selectively inhibited activation of the respiratory burst (RB) of human neutrophils in response to tumor necrosis factor (TNF) and formylated peptide but not phorbol ester and spared the ability of neutrophils to kill bacteria. These compounds partially inhibited TNF-triggered cytoskeletal rearrangements without blocking adhesion or transmigation of polymorphonuclear neutrophils through TNF-activated monolayers of endothelial cells. The compounds were nontoxic to neutrophils and endothelial cells. They had no direct inhibitory effect on the tyrosine kinases Src, Syk, or Pyk2. However, their differential effects on cell spreading, bacteria-induced RB, TNF-induced degranulation, TNF-induced protein tyrosine phosphorylation, and TNF-induced Syk activation suggested that each may act on different elements of neutrophil signaling pathways.
Regulation of matrix metalloproteinase-9 (MMP-9) in TNF-stimulated neutrophils: novel pathways for tertiary granule release
Authors: Chakrabarti Subhadeep , Zee Jennifer M , Patel Kamala D 
Published: November 2005

Abstract
Matrix metalloproteinase-9 (MMP-9) is present in the tertiary granules of neutrophils and is rapidly released following stimulation. We examined the pathways that regulate tumor necrosis factor (TNF)-mediated MMP-9 release and found this to be dependent on the TNF receptor I. TNF rapidly activated extracellular signal-regulated kinase and p38 mitogen-activated protein kinases, but neither of these pathways was critical for MMP-9 release. Many neutrophil responses to TNF require β2-integrin-dependent signaling and subsequent Src family kinase activation. In conrast, we found that MMP-9 release from tertiary granules was only partially affected by blocking β2-integrin-mediated adhesion. Similarly, blocking Src family kinases with the inhibitor PP2 only attenuated TNF-induced MMP-9 release. Blocking β2-integrin-mediated adhesion and Src family kinases did not result in additive inhibition of MMP-9 release. In contrast, inhibiting protein kinase C (PKC) with a pan-specific inhibitor blocked greater than 85% of MMP-9 release. Inhibitors against specific PKC isoforms suggested a role for PKC α and PKC δ in maximal MMP-9 release. These data suggest that MMP-9 release from tertiary granules uses β2-integrin-independent signaling pathways. Furthermore, PKC isoforms play a critical role in regulating tertiary granule release.
Elevated gelatinase activity in pulmonary alveolar proteinosis: role of macrophage-colony stimulating factor
Authors: Bonfield Tracey L , Swaisgood Carmen M , Barna Barbara P , Farver Carol F , Kavuru Mani S , Thomassen Mary Jane 
Published: November 2005

AbstractPulmonary alveolar proteinosis (PAP) is an anti-granulocyte macrophage-colony stimulating factor (GM-CSF) autoimmune disease resulting in the accumulation of phospholipids in the alveoli. GM-CSF knockout (KO) mice exhibit a strikingly similar lung pathology to patients with PAP. The lack of functionally active GM-CSF correlates with highly elevated concentrations of M-CSF in the lungs of PAP patients and GM-CSF KO mice. M-CSF has been associated with alternative macrophage activation, and in models of pulmonary fibrosis, M-CSF also contributes to tissue resorption and fibrosis. Matrix metalloproteinase-2 (MMP-2) and MMP-9 have been implicated in extracellular matrix degradation in animal models of fibrosis and asthma. We show for the first time that the lungs of PAP patients contain highly elevated levels of MMP-2 and MMP-9. PAP broncholaveolar lavage (BAL) cells but not bronchial epithelial cells expressed increased MMP-2 and MMP-9 mRNA relative to healthy controls. Both MMPs were detectable as pro and active proteins by gelatin zymography; and by fluorometric global assay, PAP–MMP activity was elevated. BAL cells/fluids from GM-CSF KO mice also demonstrated significantly elevated MMP-2 and MMP-9 gene expression, protein, and activity. Finally, PAP patients undergoing GM-CSF therapy exhibited significantly reduced MMPs and M-CSF. These data suggest that in the absence of GM-CSF, excess M-CSF in PAP may redirect alveolar macrophage activation, thus potentially contributing to elevated MMP expression in the lung.
LIGHT enhances the bactericidal activity of human monocytes and neutrophils via HVEM
Authors: Heo Sook-Kyoung , Ju Seong-A , Lee Sang-Chul , Park Sang-Min , Choe Suck-Young , Kwon Byungsuk , Kwon Byoung S , Kim Byung-Sam 
Published: November 2005

Abstract
Human monocytes and neutrophils play major roles in clearing bacteria from human blood and tissues. We found that the herpes virus entry mediator (HVEM) was highly expressed in monocytes and neutrophils, and its interaction with “homologous to lymphotoxins, shows inducible expression, and competes with herpes simplex virus glycoprotein D for HVEM/tumor necrosis factor (TNF)-related 2” (LIGHT) enhanced bactericidal activity against Listeria monocytogenes and Staphylococcus aureus. The LIGHT-HVEM interaction increased levels of phagocytosis, interleukin (IL)-8, TNF-α, nitric oxide (NO), and reactive oxygen species (ROS) in monocytes and neutrophils. Anti-HVEM monoclonal antibody was able to block LIGHT-induced bactericidal activity, cytokine production (IL-8 and TNF-α), and ROS generation. Moreover, inhibition of ROS and NO production blocked LIGHT-induced bactericidal activity. Our results indicate that the LIGHT/HVEM interaction in monocytes and neutrophils contributes to antibacterial activity.
Oxidative stress in operating room personnel: occupational exposure to anesthetic gases
Authors: Malekirad A Akbar , Ranjbar A , Rahzani K , Kadkhodaee M , Rezaie A , Taghavi B , Abdollahi M 
Published: November 2005

Health professionals exposed to anesthetic gases are at higher risk of reproductive, neurological, hematological, immunological, hepatic and renal system diseases. We investigated if oxidative stress induced by chronic exposure to anesthetic gases has any association with this matter. Plasma lipid peroxidation, total antioxidant capacity and total thiol molecule levels were measured in 66 operating room staff in comparison with 66 controls. The exposed group had a significantly higher level of lipid peroxidation with decreased thiol groups compared to control subjects. Total antioxidant capacity of the body was no different among exposed and not exposed subjects. Increased lipid peroxidation in the blood of exposed subjects warns that oxygen free radicals have increased in the body and thus might attack cells, which, in the longterm, results in multi-organ damage. The remaining blood total antioxidant capacity at normal values is promising and means that other non-thiol antioxidants, such as uric acid, transferrin, ceruloplasmin, albumin, and vitamin antioxidants, such as a-tocopherol and ascorbic acid, have been stimulated to maintain the total anti-oxidant power of the body at normal state.
Phase III Study Comparing Cisplatin Plus Fluorouracil to Paclitaxel, Cisplatin, and Fluorouracil Induction Chemotherapy Followed by Chemoradiotherapy in Locally Advanced Head and Neck Cancer
Authors: Hitt Ricardo , López-Pousa Antonio , Martínez-Trufero Javier , Escrig Vicente , Carles Joan , Rizo Alfredo , Isla Dolores , Vega M. Eugenia , Martí Juan L. , Lobo Francisco , Pastor Pedro , Valentí Vicente , Belón Joaquín , Sánchez Miguel A. , Chaib Carlos , Pallarés Cinta , Antón Antonio , Cervantes Andrés , Paz-Ares Luis , Cortés-Funes Hernán 
Published: November 2005

Purpose To compare the antitumor activity and toxicity of the two induction chemotherapy treatments of paclitaxel, cisplatin, and fluorouracil (FU; PCF) versus standard cisplatin and FU (CF), both followed by chemoradiotherapy (CRT), in locally advanced head and neck cancer (HNC). Patients and Methods Eligibility criteria included biopsy-proven, previously untreated, stage III or IV locally advanced HNC. Patients received either CF (cisplatin 100 mg/m2 on day 1 plus FU 1,000 mg/m2 continuous infusion on days 1 through 5) or PCF (paclitaxel 175 mg/m2 on day 1, cisplatin 100 mg/m2 on day 2, and FU 500 mg/m2 continuous infusion on days 2 through 6); both regimens were administered for three cycles every 21 days. Patients with complete response (CR) or partial response of greater than 80% in primary tumor received additional CRT (cisplatin 100 mg/m2 on days 1, 22, and 43 plus 70 Gy). Results A total of 382 eligible patients were randomly assigned to CF (n = 193) or PCF (n = 189). The CR rate was 14% in the CF arm v 33% in the PCF arm (P < .001). Median time to treatment failure was 12 months in the CF arm compared with 20 months in the PCF arm (log-rank test, P = .006; Tarone-Ware, P = .003). PCF patients had a trend to longer overall survival (OS; 37 months in CF arm v 43 months in PCF arm; log-rank test, P = .06; Tarone-Ware, P = .03). This difference was more evident in patients with unresectable disease (OS: 26 months in CF arm v 36 months in PCF arm; log-rank test, P = .04; Tarone-Ware, P = .03). CF patients had a higher occurrence of grade 2 to 4 mucositis than PCF patients (53% v 16%, respectively; P < .001). Conclusion Induction chemotherapy with PCF was better tolerated and resulted in a higher CR rate than CF. However, new trials that compare induction chemotherapy plus CRT versus CRT alone are needed to better define the role of neoadjuvant treatment.
Early Mortality After Diagnosis of Multiple Myeloma: Analysis of Patients Entered Onto the United Kingdom Medical Research Council Trials Between 1980 and 2002—Medical Research Council Adult Leukaemia Working Party
Authors: Augustson Bradley M. , Begum Gulnaz , Dunn Janet A. , Barth Nicola J. , Davies Faith , Morgan Gareth , Behrens Judith , Smith Alastair , Child J. Anthony , Drayson Mark T. 
Published: November 2005

Purpose Early mortality in multiple myeloma (MM) is usually attributed to combined effects of active disease and comorbid factors. We have studied early deaths in a series of large multicenter trials to assess direct causes of death, their predictability, and whether current management strategies have reduced their frequency. Patients and Methods A total of 3,107 newly diagnosed patients entered onto United Kingdom Medical Research Council MM trials from 1980 to 2002 were studied. Trial files, final clinical summaries, and postmortem reports were analyzed. Results Death within 60 days of trial entry occurred in 299 patients (10%). Logistic regression modeling identified beta 2-microglobulin, performance status, and age as the most important predictors of early death, but only with 61% sensitivity and 73% specificity. Forty-five percent of deaths were attributable to infection, which was often associated with bone pain (particularly thoracic pain) and delay in presenting to medical care. Neutropenia was present at diagnosis in only 11 of the 135 deaths from infection. Renal failure was present in 28% of early deaths and was linked to light-chain MM, hypercalcemia, dehydration, and nonsteroidal anti-inflammatory drugs. There was no time related reduction in the percentage or nature of early deaths in 1,550 patients older than 65 years receiving similar therapy between 1982 and 2002. Conclusion A tenth of patients die within 60 days of diagnosis of MM. Infection and renal failure are the main direct causes of early mortality, which cannot be accurately predicted by presenting prognostic features. All patients should be considered at high risk of death during induction therapy.