bluuebunny/crossref_metadata_2025_split huggingface dataset:
Surge Capacity Concepts for Health Care Facilities: The CO-S-TR Model for Initial Incident Assessment
Authors: Hick John L. , Koenig Kristi L. , Barbisch Donna , Bey Tareg A. 
Published: October 2008

ABSTRACTFacility-based health care personnel often lack emergency management training and experience, making it a challenge to efficiently assess evolving incidents and rapidly mobilize appropriate resources. We propose the CO-S-TR model, a simple conceptual tool for hospital incident command personnel to prioritize initial incident actions to adequately address key components of surge capacity. There are 3 major categories in the tool, each with 4 subelements. “CO” stands for command, control, communications, and coordination and ensures that an incident management structure is implemented. “S” considers the logistical requirements for staff, stuff, space, and special (event-specific) considerations. “TR” comprises tracking, triage, treatment, and transportation: basic patient care and patient movement functions. This comprehensive yet simple approach is designed to be implemented in the immediate aftermath of an incident, and complements the incident command system by aiding effective incident assessment and surge capacity responses at the health care facility level. (Disaster Med Public Health Preparedness. 2008;2(Suppl 1):S51–S57)
Mass Casualty Triage: An Evaluation of the Data and Development of a Proposed National Guideline
Authors: Lerner E. Brooke , Schwartz Richard B. , Coule Phillip L. , Weinstein Eric S. , Cone David C. , Hunt Richard C. , Sasser Scott M. , Liu J Marc , Nudell Nikiah G. , Wedmore Ian S. , Hammond Jeffrey , Bulger Eileen M. , Salomone Jeffrey P. , Sanddal Teri L. , Lord Graydon C. , Markenson David , O'Connor Robert E. 
Published: October 2008

ABSTRACTMass casualty triage is a critical skill. Although many systems exist to guide providers in making triage decisions, there is little scientific evidence available to demonstrate that any of the available systems have been validated. Furthermore, in the United States there is little consistency from one jurisdiction to the next in the application of mass casualty triage methodology. There are no nationally agreed upon categories or color designations. This review reports on a consensus committee process used to evaluate and compare commonly used triage systems, and to develop a proposed national mass casualty triage guideline. The proposed guideline, entitled SALT (sort, assess, life-saving interventions, treatment and/or transport) triage, was developed based on the best available science and consensus opinion. It incorporates aspects from all of the existing triage systems to create a single overarching guide for unifying the mass casualty triage process across the United States. (Disaster Med Public Health Preparedness. 2008;2(Suppl 1):S25–S34)
Disaster Triage Systems for Large-scale Catastrophic Events
Authors: Bostick Nathan A. , Subbarao Italo , Burkle Frederick M. , Hsu Edbert B. , Armstrong John H. , James James J. 
Published: October 2008

ABSTRACTLarge-scale catastrophic events typically result in a scarcity of essential medical resources and accordingly necessitate the implementation of triage management policies to minimize preventable morbidity and mortality. Accomplishing this goal requires a reconceptualization of triage as a population-based systemic process that integrates care at all points of interaction between patients and the health care system. This system identifies at minimum 4 orders of contact: first order, the community; second order, prehospital; third order, facility; and fourth order, regional level. Adopting this approach will ensure that disaster response activities will occur in a comprehensive fashion that minimizes the patient care burden at each subsequent order of intervention and reduces the overall need to ration care. The seamless integration of all orders of intervention within this systems-based model of disaster-specific triage, coordinated through health emergency operations centers, can ensure that disaster response measures are undertaken in a manner that is effective, just, and equitable. (Disaster Med Public Health Preparedness. 2008;2(Suppl 1):S35–S39)
Participatory Action Research Methodology in Disaster Research: Results From the World Trade Center Evacuation Study
Authors: Gershon Robyn R.M. , Rubin Marcie S. , Qureshi Kristine A. , Canton Allison N. , Matzner Frederick J. 
Published: October 2008

ABSTRACTObjective: Participatory action research (PAR) methodology is an effective tool in identifying and implementing risk-reduction interventions. It has been used extensively in occupational health research, but not, to our knowledge, in disaster research. A PAR framework was incorporated into the World Trade Center evacuation study, which was designed to identify the individual, organizational, and structural (environmental) factors that affected evacuation from the World Trade Center Towers 1 and 2 on September 11, 2001. PAR teams—comprising World Trade Center evacuees, study investigators, and expert consultants—worked collaboratively to develop a set of recommendations designed to facilitate evacuation from high-rise office buildings and reduce risk of injury among evacuees.Methods: Two PAR teams worked first separately and then collectively to identify data-driven strategies for improvement of high-rise building evacuation.Results: The teams identified interventions targeting individual, organizational, and structural (environmental) barriers to safe and rapid evacuation.Conclusions: PAR teams were effective in identifying numerous feasible and cost-effective strategies for improvement of high-rise emergency preparedness and evacuation. This approach may have utility in other workplace disaster prevention planning and response programs. (Disaster Med Public Health Preparedness. 2008;2:142–149)
Leishmania donovaniinfection down-regulates TLR2-stimulated IL-12p40 and activates IL-10 in cells of macrophage/monocytic lineage by modulating MAPK pathways through a contact-dependent mechanism
Authors: Chandra Dinesh , Naik Sita 
Published: October 2008

SummaryThe failure of Leishmania, an intracellular pathogen, to stimulate a pro-inflammatory response following entry into macrophages has been well reported. This occurs in spite of the fact that ligands for the toll-like receptors (TLR) have been recently shown on the parasite surface and their role in disease protection well documented. The outcome of infection in leishmaniasis is determined by the Th1 versus Th2 nature of the effector response and the generation of IL-12 and IL-10 by the infected macrophages is important for this decision. We evaluated the effect of L. donovani infection of monocytes (cell line THP-1, and monocytes derived from human peripheral blood) on Pam3cys (TLR2 ligand) and lipopolysaccharide (TLR4 ligand) stimulated production of IL-12p40 and IL-10. L. donovani infection caused suppression of TLR2 and TLR4-stimulated IL-12p40, with an increase in IL-10 production. Parasites also modulated the TLR2-stimulated mitogen-activated protein kinase (MAPK) pathway by suppressing MAPK P38 phosphorylation and activating extracellular regulated kinase (ERK)1/2 phosphorylation. These effects could be reversed either by using a MAPK P38 activator, anisomycin, or ERK1/2 inhibitor, U0126. L. donovani caused modulation of TLR2-stimulated MAPK pathways in a contact-dependent mechanism. In addition parasite structural integrity but not viability was required for suppression of TLR2-stimulated IL-12p40 and activation of IL-10. These observations suggest that L. donovani has evolved survival strategies that subvert the pro-inflammatory response generated through TLRs.
Impaired immune responses in streptozotocin-induced type I diabetes in mice. Involvement of high glucose
Authors: Rubinstein R , Genaro A M , Motta A , Cremaschi G , Wald M R 
Published: October 2008

SummaryDiabetes is widely believed to predispose to serious infections. However, the mechanisms linking diabetes and immunosuppression are not well defined. One potential mediator of the altered defence mechanisms is hyperglycaemia. It has been identified as the main factor contributing to the development of diseases associated with diabetes mellitus. In this study we analyse the immune response in diabetes and the direct effect of hyperglycaemia on T and B lymphocyte reactivity. Diabetes induced an early decrease in IgG levels in the secondary response. However, both primary responses against a T-cell-dependent or independent antigen were affected after 6 months of diabetes induction. T- and B- cell proliferation was only decreased at this time. To gain insight into the potential mechanisms involved, we evaluated the influence of hyperglycaemia over the immune response. Pre-incubation of lymph node and spleen cells in a high glucose (HG) containing medium led to a significant time- and dose-dependent decrease in T- and B-cell proliferation. This effect was associated with the presence of HG-derived supernatants. Still viable cells after HG exposition were able to improve their proliferative response when cultured with the mitogen in a fresh standard medium. HG diminished cell viability, increased apoptosis and induced oxidative stress in lymphocytes. These results indicate that HG concentrations can directly affect lymphoid cell growth. An increase in oxidative stress would be implicated in this deleterious effect. The possibility that prolonged exposure to pathologically HG concentrations would result in the immunosuppressive state observed in diabetes is also discussed.
A RNA transcript (Heg) in mononuclear cells is negatively correlated with CD14 mRNA and TSH receptor autoantibodies
Authors: Christensen N J , Habekost G , Bratholm P 
Published: October 2008

Summary
During a study of gene expression of foxp3 in blood mononuclear cells we observed a DNA product of an unknown RNA fragment. The area of this peak correlated with CD14 mRNA in a small group of subjects. The sequence was localized to chromosome 1. We tested the hypothesis that gene expression of the poly A(−) transcript (designated Heg) in mononuclear cells was correlated with CD14 mRNA in normal subjects and with CD14 mRNA and TSH receptor autoantibodies in patients with acute and untreated Graves' disease. mRNA was expressed in amol/µg DNA. The main study groups were: (i) normal subjects; (ii) patients with early and untreated Graves' disease; and (iii) patients with Graves' disease studied after treatment. In 18 normal subjects and in 20 patients with treated Graves' disease CD14 mRNA was negatively correlated with Heg (P &lt; 0·001). In 17 untreated patients with Graves' disease Heg and thyroid receptor autoantibodies were negatively correlated (P &lt; 0·009). Incubation studies with mononuclear cells showed that the addition of a fragment of the central part of Heg (949 bases) to mononuclear cells decreased CD14 mRNA markedly to zero or nearly zero (P &lt; 0·001). This response was not specific in the sense that siRNA and lipopolysaccharide also decreased CD14 mRNA, probably due to activation of the CD14/Toll-like receptor complex. Single-stranded RNA is likely to increase interferon production. Due to the anti-inflammatory effect Heg may also inhibit the early phase of TSH receptor autoantibody production.
Expression of the CXCR6 on polymorphonuclear neutrophils in pancreatic carcinoma and in acute, localized bacterial infections
Authors: Gaida M M , Günther F , Wagner C , Friess H , Giese N A , Schmidt J , Hänsch G M , Wente M N 
Published: October 2008

Summary
The chemokine receptor CXCR6 has been described on lymphoid cells and is thought to participate in the homing of activated T-cells to non-lymphoid tissue. We now provide evidence that the chemokine receptor CXCR6 is also expressed by activated polymorphonuclear neutrophils (PMN) in vivo: Examination of biopsies derived from patients with pancreatic carcinoma by confocal laser scan microscopy revealed a massive infiltration of PMN that expressed CXCR6, while PMN of the peripheral blood of these patients did not. To answer the question whether CXCR6 expression is a property of infiltrated and activated PMN, leucocytes were collected from patients with localized soft tissue infections in the course of the wound debridement. By cytofluorometry, the majority of these cells were identified as PMN. Up to 50% of these PMN were also positive for CXCR6. Again, PMN from the peripheral blood of these patients were nearly negative for CXCR6, as were PMN of healthy donors. In a series of in vitro experiments, up-regulation of CXCR6 on PMN of healthy donors by a variety of cytokines was tested. So far, a minor, although reproducible, effect of tumour necrosis factor (TNFα) was seen: brief exposure with low-dose TNFα induced expression of CXCR6 on the surface of PMN. Furthermore, we could show an increased migration of PMN induced by the axis CXCL16 and CXCR6. In summary, our data provide evidence that CXCR6 is not constitutively expressed on PMN, but is up-regulated under inflammatory conditions and mediates migration of CXCR6-positive PMN.
Anti-oxLDL antibody isotype levels, as potential markers for progressive atherosclerosis in APOE−/− and APOE−/−CD40L−/− mice
Authors: Smook M L F , van Leeuwen M , Heeringa P , Damoiseaux J G M C , Theunissen R , Daemen M J A P , Lutgens E , Cohen Tervaert J W 
Published: October 2008

Summary
In humans and animal models of atherosclerosis, antibodies against oxidized LDL have been associated with atherosclerotic lesion development. It has been suggested that IgM anti-oxLDL antibodies are anti-atherogenic, whereas IgG anti-oxLDL antibodies are pro-atherogenic. In this study, we examined the relation between IgM and IgG antibody levels and atherosclerosis severity in APOE−/−CD40L−/− mice, which are deficient for IgG and develop moderate advanced atherosclerosis, and compared results with mice developing severe (APOE−/−) or no atherosclerosis (C57Bl/6). Mice were followed in time for anti-oxLDL antibodies while on high-fat diet or normal chow. Anti-oxLDL antibody levels were determined by ELISA. Results revealed that 24-week-old APOE−/−CD40L−/− mice had enhanced IgM anti-oxLDL antibody levels when compared with wild-type mice, but similar levels to those of APOE−/− mice. As expected, IgG anti-oxLDL antibody levels were almost absent in APOE−/−CD40L−/− mice. The transition from early to advanced lesions in APOE−/− mice was reflected by elevated IgM anti-oxLDL antibody levels. IgM anti-oxLDL levels did not further increase during progression to more advanced lesions. No relation was found between IgG anti-oxLDL levels and atherosclerosis severity. In conclusion, the severity of advanced atherosclerosis in mice is not reflected by IgM and/or IgG anti-oxLDL antibody levels. Furthermore, less advanced atherosclerotic lesion development in APOE−/−CD40L−/− mice does not seem to be the result of higher levels of protective IgM anti-oxLDL antibodies. Therefore, our study does not support the idea that the previously observed inconsistency in the relation between anti-oxLDL and atherosclerosis severity is due to differences in antibody isotypes.
B cells are involved in the modulation of pathogenic gut immune response in food-allergic enteropathy
Authors: Cardoso C R , Provinciatto P R , Godoi D F , Vieira T S , Ferreira B R , Teixeira G , Rossi M A , Cunha F Q , Silva J S 
Published: October 2008

SummaryFood enteropathies involve uncontrolled or hypersensitivity reactions to ingested nutrients and may result in IgE and T-helper type 2 (Th2) responses as in food allergy. However, the precise role of B cells in the development of food enteropathies remains uncertain. In this work, we used B cell-deficient mice (B KO) and a model of peanut sensitization to examine the involvement of B lymphocytes in the pathogenesis of food allergy. Results showed that priming of wild-type (WT) mice with peanut proteins induced specific IgG1 and IgE responses in serum, with edema, tissue destruction, epithelial exulceration and inflammatory infiltrate in the gut of sensitized and challenged (S + Peanut) WT animals. In contrast, there was no sera immunoglobulin detection and absence of tissue destruction in the gut of B KO mice, which presented moderate inflammatory infiltrate and villous enlargement after peanut challenge. These animals presented marked decrease in IL-4 and TNF-α and high levels of IL-10, TGF-β, IL-12p40 and IFN-γ mRNA in the gut. Moreover, the expression of CCL5, CCL11 and CXCL1 was reduced in the gut of B KO mice, in contrast to elevated messages of CCL2 or similar detection of Th1-related chemokines in S + Peanut WT mice. Finally, we provided evidence that B cells are necessary to the development of food-related enteropathies and induction of gut inflammation during allergic reactions to food.
Non-obese diabetic–recombination activating gene-1 (NOD–Rag 1 null) interleukin (IL)-2 receptor common gamma chain (IL 2 rγnull) null mice: a radioresistant model for human lymphohaematopoietic engraftment
Authors: Pearson T , Shultz L D , Miller D , King M , Laning J , Fodor W , Cuthbert A , Burzenski L , Gott B , Lyons B , Foreman O , Rossini A A , Greiner D L 
Published: October 2008

SummaryImmunodeficient hosts engrafted with human lymphohaematopoietic cells hold great promise as a preclinical bridge for understanding human haematopoiesis and immunity. We now describe a new immunodeficient radioresistant non-obese diabetic mice (NOD) stock based on targeted mutations in the recombination activating gene-1 (Rag1null) and interleukin (IL)-2 receptor common gamma chain (IL2rγnull), and compare its ability to support lymphohaematopoietic cell engraftment with that achieved in radiosensitive NOD.CB17–Prkdcscid (NOD–Prkdcscid) IL2rγnull mice. We observed that immunodeficient NOD–Rag1null IL2rγnull mice tolerated much higher levels of irradiation conditioning than did NOD–Prkdcscid IL2rγnull mice. High levels of human cord blood stem cell engraftment were observed in both stocks of irradiation-conditioned adult mice, leading to multi-lineage haematopoietic cell populations and a complete repertoire of human immune cells, including human T cells. Human peripheral blood mononuclear cells also engrafted at high levels in unconditioned adult mice of each stock. These data document that Rag1null and scid stocks of immunodeficient NOD mice harbouring the IL2rγnull mutation support similar levels of human lymphohaematopoietic cell engraftment. NOD–Rag1null IL2rγnull mice will be an important new model for human lymphohaematopoietic cell engraftment studies that require radioresistant hosts.
Distribution of immunoglobulin G subclasses of anti-thyroid peroxidase antibody in sera from patients with Hashimoto's thyroiditis with different thyroid functional status
Authors: Xie L-D , Gao Y , Li M-R , Lu G-Z , Guo X-H 
Published: October 2008

SummaryThe mechanism of disease progression in Hashimoto's thyroiditis (HT) is still unclear. Anti-thyroid peroxidase antibody (TPOAb), a diagnostic hallmark of HT, is principally of the immunoglobulin G (IgG) isotype, and it appears to be a response to thyroid injury. The aim of our study was to evaluate the distribution of IgG subclasses of TPOAb in sera from patients with HT with different thyroid functional status. Sera from 168 patients with newly diagnosed HT were collected and divided into three groups according to thyroid function: patients with hypothyroidism (n = 66), subclinical hypothyroidism (n = 60) and euthyroidism (n = 42). Antigen-specific enzyme-linked immunosorbent assay was used to detect the distribution of TPOAb IgG subclasses. The prevalence of TPOAb IgG subclasses in all patients’ sera with HT was IgG1 70·2%, IgG2 35·1%, IgG3 19·6% and IgG4 66·1% respectively. The prevalence of IgG2 in sera from patients with hypothyroidism (51·5%) was significantly higher than that of subclinical hypothyroidism (33·3%) (P &lt; 0·05), and the latter was also significantly higher than that of euthyroidism (11·9%) (P &lt; 0·05). The positive percentage of IgG2 subclass in sera from patients with hypothyroidism and subclinical hypothyroidism was significantly higher than that of euthyroidism (P &lt; 0·05), the prevalence and positive percentage of IgG4 subclass in sera from patients with hypothyroidism and subclinical hypothyroidism was significantly higher than that of euthyroidism respectively (P &lt; 0·05). The predominant TPOAb IgG subclasses in sera from patients with HT were IgG1 and IgG4. Patients with high levels of TPOAb IgG2, IgG4 subclasses might be at high risk of developing overt hypothyroidism.
Overexpression of interleukin-12 and T helper 1 predominance in lupus nephritis
Authors: Tucci M , Lombardi L , Richards H B , Dammacco F , Silvestris F 
Published: October 2008

SummaryImbalance of cytokine homeostasis is a prominent feature of both experimental and human systemic lupus erythematosus (SLE). Because interleukin (IL)-12 promotes interferon (IFN)-γ production leading to polarization of peripheral cells toward a T helper (Th) 1 phenotype, we investigated its role in lupus nephritis (LN). Soluble Th1 and Th2 cytokines were measured by enzyme-linked immunosorbent assay (ELISA) in sera and urines of SLE patients and controls. Th1/Th2 peripheral lymphocyte polarization was determined by flow cytometry. Glomerular accumulation of IL-12 was evaluated by immunohistochemistry, whereas urinary IL-12 was evaluated by ELISA. Higher serum IL-12 levels in SLE were associated with LN, whereas IL-4 was unrelated to the renal damage. Peripheral cells from LN patients showed a Th1 phenotype with a high IFN-γ expression that paralleled the severity of renal damage. IL-12 was present within glomerular mononuclear cells in classes IV and V LN, and its accumulation was correlated strongly with urinary levels. IL-12 overexpression in SLE may contribute to the development of LN. Both serum and urinary IL-12 elevation reflect its glomerular production and parallel Th1 polarization of peripheral T cells and high IFN-γ production. In SLE patients, IL-12 measurement may thus be predictive of the development of LN.
Effect of proteolytic activity ofEpicoccum purpurascensmajor allergen, Epi p 1 in allergic inflammation
Authors: Kukreja N , Sridhara S , Singh B P , Arora N 
Published: October 2008

SummaryEnzymes play an important role in inducing airway inflammation, but knowledge is limited to few proteins. This study was carried out to assess the role of Epi p 1, a serine protease of Epicoccum purpurascens, in inducing allergy and inflammation in a murine model. Balb/c mice were sensitized with Epi p 1 active protease (EAP) or Epicoccum extract. Subsequently, Epi p 1 sensitized mice were boosted on day 14 with EAP or inactivated protease (EIAP). Three intranasal challenges were given and mice were killed to obtain blood, bronchoalveolar lavage fluid (BALF), spleen and lung tissues. Cellular airways infiltration, immunoglobulin E (Ig)E titres and cytokine levels in BALF and splenocyte culture supernatant were compared. Mice immunized with EAP had higher Epi p 1-specific serum IgE and IgG1 than EIAP immunized mice (P &lt; 0·01). There was a twofold difference in the number of eosinophils in BALF of EAP mice and EIAP mice (P &lt; 0·01). A similar trend was recorded for eosinophil peroxidase activity (P &lt; 0·05), indicating the role of proteolytic activity in inducing inflammation. Further, lung histology revealed increased leucocyte infiltration and airway narrowing, with higher inflammation scores in the EAP group than in the EIAP group. The lungs of EAP mice showed increased mucus and goblet cell metaplasia. Interleukin (IL)-4 and IL-5 levels were higher in BALF and splenocyte culture supernatant of EAP mice than in EIAP mice (P &lt; 0·05), indicating a T helper 2 response. Proteolytic activity of Epi p 1 plays an important role in inducing allergic inflammation. The enzymatically inactive form may be investigated for immunotherapy.