Nesta pesquisa foi avaliada a incidência e a severidade da mucosite oral em pacientes que foram submetidos à adequação bucal previamente ao Transplante de Medula Óssea. Foi realizado exame clínico e radiográfico dos pacientes portadores de Leucemia Mielóide Crônica que estavam se preparando para o transplante. Após a avaliação inicial dos pacientes foram realizados os tratamentos odontológicos necessários para a remoção de quaisquer focos de infecção bucal. Todos os pacientes receberam o mesmo tipo de condicionamento quimioterápico e de profilaxia para Doença do Enxerto-Contra-Hospedeiro. Todos os pacientes receberam adequação bucal e foram avaliados durante o período de internação hospitalar para o transplante pelo mesmo Cirurgião Dentista. Os resultados mostraram que a mucosite grau 0 foi encontrada em 5 pacientes (14,29%), grau 1 em 8 pacientes (22,85%), grau 2 em 17 pacientes (48,57%), grau 3 em 3 pacientes (8,57%) e grau 4 em 2 pacientes (5,71%). Estes dados sugerem que a adequação bucal realizada previamente ao Transplante de Medula Óssea reduziu a severidade da mucosite oral, salientando a importância da presença do Cirurgião Dentista na equipe multidisciplinar em um serviço de Transplante de Medula Óssea. / The aim of this research was to evaluate the incidence and the severity of the oral mucositis in patients submitted to dental treatment before the Bone Marrow Transplantation. Clinical and radiographical examination was performed in patients with Chronic Myeloid Leukemia who would be submitted to transplantation. After patient’s initial evaluation, dental treatment was performed in order to remove any site of oral infection. All patients received the same chemotherapy conditioning regimen and the Graft-versus-host-disease prophylaxis. All patients received oral care during the hospital intern period and were evaluated by the same dentist. The results showed that 5 patients (14,29%) presented level 0 of oral mucositis, 8 patients (22,85%) presented level 1 of oral mucositis were, 17 patients (48,57%) presented level 3 of oral mucositis and 2 patients (5,71%) presented level 4 of oral mucositis. These data suggest that oral care and dental treatment previous to the Bone Marrow Transplantation reduced the severity of oral mucositis and emphasizes the importance of the Dentist as a member of a multidisciplinary team in a Bone Marrow Transplantation unit.

Lee, Hoi Ying. / "September 2010." / Thesis (M.Phil.)--Chinese University of Hong Kong, 2010. / Includes bibliographical references (leaves 171-189). / Abstracts in English and Chinese. / Abstract (English) --- p.i / Abstract (Chinese) --- p.iii / Acknowledgement --- p.v / Publications --- p.vi / Abbreviations --- p.vii / Table of Content --- p.x / Chapter 1 --- Introduction --- p.1 / Chapter 1.1 --- Human mast cells and its activation --- p.1 / Chapter 1.2 --- Role of mast cells in inflammation --- p.2 / Chapter 1.3 --- Mast cell heterogeneity --- p.5 / Chapter 1.4 --- Interaction of bone and immune system --- p.1 / Chapter 1.5 --- Introduction of bone system --- p.8 / Chapter 1.6 --- Bone remodeling --- p.9 / Chapter 1.7 --- Regulation of bone remodeling --- p.10 / Chapter 1.8 --- Introduction of Osteoporosis --- p.12 / Chapter 1.9 --- Pathophysiology of osteoporosis --- p.13 / Chapter 1.10 --- Pharmacological interventions in osteoporosis --- p.14 / Chapter 1.11 --- Involvement of mast cells in bone metabolism --- p.18 / Chapter 1.12 --- Aim of study --- p.20 / Chapter 2 --- Materials and Methods --- p.27 / Chapter 2.1 --- Materials --- p.27 / Chapter 2.2 --- Methods --- p.34 / Chapter 2.2.1 --- Human mast cells culture --- p.34 / Chapter 2.2.2 --- Human mast cells characterization --- p.35 / Chapter 2.2.3 --- Histamine release assay --- p.36 / Chapter 2.2.4 --- Immunofluorescence staining of estrogen receptors --- p.37 / Chapter 2.2.5 --- Reverse Transcriptase Polymerase Chain Reaction --- p.37 / Chapter 2.2.6 --- TNF measurement --- p.38 / Chapter 2.2.7 --- Calcium mobilization studies of mast cells --- p.38 / Chapter 2.2.8 --- Statistical analysis --- p.39 / Chapter 3 --- Effects of estrogen and selective estrogen receptor modulators (SERMs) on mediators release from human mast cells --- p.41 / Chapter 3.1 --- Introduction --- p.41 / Chapter 3.2 --- Materials and methods --- p.50 / Chapter 3.3 --- Results --- p.51 / Chapter 3.3.1 --- Characterization of human mast cells --- p.51 / Chapter 3.3.2 --- Effect of estrogen on mediator release from human mast cells --- p.52 / Chapter 3.3.2.1 --- Basal histamine release after treatment of estrogen --- p.52 / Chapter 3.3.2.2 --- Histamine release induced by immunological stimulus --- p.52 / Chapter 3.3.2.3 --- Histamine release induced by chemical secretagogues --- p.54 / Chapter 3.3.3 --- Effect of selective estrogen receptor modulators (SERMs) on mast cell activity --- p.54 / Chapter 3.3.3.1 --- Basal histamine release after SERMs treatment --- p.54 / Chapter 3.3.3.2 --- Histamine release induced by immunological stimulus --- p.55 / Chapter 3.3.3.3 --- Histamine release induced by chemical secretagogues --- p.57 / Chapter 3.3.4 --- Effect of estradiol on TNF-α release from human mast cells --- p.57 / Chapter 3.3.5 --- Effect of SERMs on TNE-α release from human mast cells --- p.58 / Chapter 3.3.6 --- Expression of estrogen receptors on human mast cells --- p.59 / Chapter 3.3.6.1 --- Expression of estrogen receptor after treatment of estradiol --- p.59 / Chapter 3.3.7 --- Expression of various bone remodeling molecules on human mast cells --- p.60 / Chapter 3.3.7.1 --- Expression of bone remodeling molecule after treatment of estradiol --- p.61 / Chapter 3.4 --- Discussion --- p.63 / Chapter 4 --- Effects of anti-osteoporosis Chinese herbal medicines on activity of human mast cells --- p.98 / Chapter 4.1 --- Introduction --- p.98 / Chapter 4.2 --- Materials and methods --- p.103 / Chapter 4.3 --- Results --- p.104 / Chapter 4.3.1 --- Effect of the anti-osteoporosis Chinese herbal formulation ELP on histamine release from human mast cells --- p.104 / Chapter 4.3.1.1 --- Histamine release induced by immunological stimulus --- p.104 / Chapter 4.3.1.2 --- Histamine release induced by chemical secretagogues --- p.105 / Chapter 4.3.2 --- Effect of Herba Epimedii (HEP) on histamine release from human mast cells --- p.105 / Chapter 4.3.2.1 --- Histamine release induced by immunological stimulus --- p.106 / Chapter 4.3.2.2 --- Histamine release induced by chemical secretagogues --- p.106 / Chapter 4.3.3 --- Effect of Fructus Ligustri Lucidi (FLL) on histamine release from human mast cells --- p.107 / Chapter 4.3.3.1 --- Histamine release induced by immunological stimulus --- p.107 / Chapter 4.3.3.2 --- Histamine release induced by chemical secretagogues --- p.107 / Chapter 4.3.4 --- Effect of Fructus Psoraleae (FP) on histamine release from human mast cells --- p.108 / Chapter 4.3.4.1 --- Histamine release induced by immunological stimulus --- p.108 / Chapter 4.3.4.2 --- Histamine release induced by chemical secretagogues --- p.109 / Chapter 4.3.5 --- Effect of various partitions from solvent extraction of HEP on histamine release from human mast cells --- p.109 / Chapter 4.3.5.1 --- Histamine release induced by immunological stimulus --- p.110 / Chapter 4.3.5.2 --- Histamine release induced by chemical secretagogue --- p.111 / Chapter 4.3.6 --- Effect of various partitions from solvent extraction of FLL on histamine release from human mast cells --- p.112 / Chapter 4.3.6.1 --- Histamine release induced by immunological stimulus --- p.113 / Chapter 4.3.6.2 --- Histamine release induced by chemical secretagogue --- p.114 / Chapter 4.3.7 --- Effect of ELP and its herbal constituents on the production of cytokine from human mast cells --- p.115 / Chapter 4.3.8 --- Modulation in calcium mobilization in activated human mast cell by ELP and its herbal constituents --- p.117 / Chapter 4.4 --- Discussion --- p.119 / Chapter 5 --- General discussion --- p.163 / Reference --- p.171

Chow, Wing Shan. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2009. / Includes bibliographical references (leaves 118-129). / Abstract also in Chinese. / Abstract --- p.i / 摘要 --- p.iv / Acknowledgements --- p.viii / Table of Contents --- p.ix / List of Tables --- p.xiii / List of Figures --- p.xv / List of Abbreviations --- p.xviii / Chapter Chapter 1 --- General Introduction --- p.1 / Chapter 1.1 --- Pesticide contaminations in the environment --- p.1 / Chapter 1.2 --- Pesticides --- p.1 / Chapter 1.2.1 --- Usage of pesticide in the world --- p.1 / Chapter 1.2.2 --- Organochlorine (OC) pesticides --- p.3 / Chapter 1.2.3 --- Organophosphate (OP) pesticides --- p.4 / Chapter 1.2.4 --- Carbamate pesticides: --- p.6 / Chapter 1.2.5 --- Pyrethroid pesticides: --- p.6 / Chapter 1.3 --- Toxicological model: Zebrafish --- p.7 / Chapter 1.4 --- Biomarkers --- p.9 / Chapter 1.4.1 --- Cytochrome P450 1A (CYP1A) --- p.12 / Chapter 1.4.2 --- Cytochrome P450 3A65 (CYP3A65) --- p.14 / Chapter 1.4.3 --- Biomarker for estrogenicity - Vitellogenin (VTG1) --- p.15 / Chapter 1.4.4 --- Catalase (CAT) and Glutathione S-transferase (GST) --- p.18 / Chapter 1.4.4.1 --- Catalase (CAT) --- p.18 / Chapter 1.4.4.2 --- Glutathion S-transferase (GST) --- p.19 / Chapter 1.4.5 --- Multiple Drug Resistance (MDR1) --- p.20 / Chapter 1.4.6 --- Acetylcholinesterase (AChE) --- p.21 / Chapter 1.5 --- Objectives of this study --- p.26 / Chapter Chapter 2 --- "Toxicity assay and biomarker studies on zebrafish embryo-larvae exposed to organochlorine pesticides: endosulfan, heptachlor and methoxychlor" --- p.28 / Chapter 2.1 --- Introduction --- p.28 / Chapter 2.2 --- Materials and methods --- p.30 / Chapter 2.2.1 --- Chemicals tested --- p.30 / Chapter 2.2.2 --- Zebrafish cultivation and egg production --- p.30 / Chapter 2.2.3 --- Determination of 96h-EC50 and 96h-LC50 of organochlorine pesticides and bisphenol-A for zebrafish embryo-larvae --- p.31 / Chapter 2.2.4 --- Pesticide exposure for determination of mRNA levels of biomarkers --- p.31 / Chapter 2.2.5 --- Extraction of total RNA from the exposed embryo-larvae samples --- p.32 / Chapter 2.2.6 --- Reverse Transcription --- p.33 / Chapter 2.2.7 --- Quantifications of mRNA levels by qPCR --- p.35 / Chapter 2.2.7.1 --- Primer design --- p.35 / Chapter 2.2.7.2 --- Validation of qPCR conditions --- p.36 / Chapter 2.2.7.3 --- Quantification of biomarker gene expression levels in zebrafish embryo-larvae --- p.42 / Chapter 2.2.8 --- Statistical analysis --- p.43 / Chapter 2.3. --- Results --- p.44 / Chapter 2.3.1 --- Toxicities of OC pesticides and bisphenol-A --- p.44 / Chapter 2.3.2 --- Effects of OC pesticides and bisphenol-A on biomarker gene expression levels --- p.44 / Chapter 2.4. --- Discussions --- p.60 / Chapter 2.4.1 --- Toxicities of OC pesticides and bisphenol-A --- p.60 / Chapter 2.4.2 --- Effects of OC pesticides on CYP1A gene expression --- p.61 / Chapter 2.4.3 --- Effects of OC pesticides on CYP3A65 gene expression --- p.61 / Chapter 2.4.4 --- Effects of OC pesticides on VTG1 gene expression --- p.63 / Chapter 2.4.5 --- Effects of OC pesticides on MDR1 gene expression --- p.64 / Chapter 2.5 --- Conclusion --- p.65 / Chapter Chapter 3 --- "Toxicity assay and biomarker studies on zebrafish embryo-larvae exposed to a organochlorine pesticide, chlorpyrifos" --- p.66 / Chapter 3.1 --- Introduction --- p.66 / Chapter 3.2 --- Materials and methods --- p.68 / Chapter 3.2.1 --- Chemicals tested --- p.68 / Chapter 3.2.2 --- Zebrafish cultivation and egg production --- p.68 / Chapter 3.2.3 --- Determination of 96h-EC50 and 96h-LC50 of chlorpyrifos for zebrafish embryo-larvae --- p.68 / Chapter 3.2.4 --- Pesticide exposure for determination of mRNA levels of biomarkers --- p.68 / Chapter 3.2.5 --- Extraction of total RNA from the exposed embryo-larvae samples --- p.69 / Chapter 3.2.6 --- Reverse Transcription --- p.69 / Chapter 3.2.7 --- Quantifications of mRNA levels by qPCR --- p.70 / Chapter 3.2.7.1 --- Primer design --- p.70 / Chapter 3.2.7.2 --- Validation of qPCR conditions --- p.70 / Chapter 3.2.7.3 --- Quantification of biomarker gene expression levels in zebrafish embryo-larvae --- p.75 / Chapter 3.2.8 --- Determination of acetylcholinesterase (AChE) activities --- p.76 / Chapter 3.2.9 --- Statistical analysis --- p.77 / Chapter 3.3 --- Results --- p.78 / Chapter 3.3.1 --- Toxicities of chlorpyrifos --- p.78 / Chapter 3.3.2 --- Effects of chlorpyrifos on CAT and GST gene expression levels --- p.81 / Chapter 3.3.3 --- Effects of chlorpyrifos on acetylcholinesterase (AChE) activity --- p.83 / Chapter 3.4 --- Discussions --- p.86 / Chapter 3.4.1 --- Toxicity of chlorpyrifos --- p.86 / Chapter 3.4.2 --- Effect of chlorpyrifos on CAT and GST gene expressions --- p.86 / Chapter 3.4.3 --- Effect of chlorpyrifos on AChE activity --- p.88 / Chapter 3.5 --- Conclusions --- p.89 / Chapter Chapter 4 --- Toxicity assay and biomarker studies on zebrafish embryo-larvae exposed to carbamate and pyrethroid pesticides --- p.90 / Chapter 4.1 --- Introduction --- p.90 / Chapter 4.2 --- Materials and methods --- p.92 / Chapter 4.2.1 --- Chemicals tested --- p.92 / Chapter 4.2.2 --- Zebrafish cultivation and egg production --- p.92 / Chapter 4.2.3 --- Determination of 96h-EC50 and 96h-LC50 of aldicarb and cypermethrin for zebrafish embryo-larvae --- p.92 / Chapter 4.2.4 --- Pesticide exposure for determination of mRNA levels of biomarkers --- p.92 / Chapter 4.2.5 --- Quantification of biomarker gene expression levels in zebrafish embryo- larvae and Determination of acetylcholinesterase (AChE) activity --- p.94 / Chapter 4.2.6 --- Statistical analysis --- p.94 / Chapter 4.3 --- Results --- p.95 / Chapter 4.3.1 --- Toxicities of aldicarb and cypermethrin --- p.95 / Chapter 4.3.2 --- Effects of aldicarb and cypermethrin on CAT and GST gene expression levels.. --- p.99 / Chapter 4.3.3 --- Effects of aldicarb on acetylcholinesterase (AChE) activity --- p.102 / Chapter 4.4 --- Discussion --- p.105 / Chapter 4.4.1 --- Toxicity of aldicarb of cypermethrin --- p.105 / Chapter 4.4.2 --- Effect of aldicarb and cypermethrin on CAT and GST gene expressions --- p.105 / Chapter 4.4.3 --- Effect of aldicarb on AChE activity --- p.107 / Chapter 4.5 --- Conclusion --- p.108 / Chapter Chapter 5 --- General Conclusion --- p.109 / Chapter 5.1 --- Toxicities of pesticides --- p.109 / Chapter 5.2 --- Effects of OC pesticides on biomarker gene expressions --- p.113 / Chapter 5.3 --- "Effects of chlorpyrifos, aldicarb and cypermetrhin on biomarker gene expressions" --- p.116 / Chapter 5.4 --- Effect of chlorpyrifos and aldicarb on AChE activity --- p.116 / References --- p.118

The link between poverty and children’s health is well recognized. Even temporary poverty may have an adverse effect on children’s health, and data consistently support the observation that poverty in childhood continues to have a negative effect on health into adulthood. In addition to childhood morbidity being related to child poverty, epidemiologic studies have documented a mortality gradient for children aged 1 to 15 years (and adults), with poor children experiencing a higher mortality rate than children from higher-income families. The global great recession is only now very slowly abating for millions of America’s children and their families. At this difficult time in the history of our nation’s families and immediately after the 50th anniversary year of President Lyndon Johnson’s War on Poverty, it is particularly germane for the American Academy of Pediatrics, which is “dedicated to the health of all children,” to publish a research-supported technical report that examines the mediators associated with the long-recognized adverse effects of child poverty on children and their families. This technical report draws on research from a number of disciplines, including physiology, sociology, psychology, economics, and epidemiology, to describe the present state of knowledge regarding poverty’s negative impact on children’s health and development. Children inherit not only their parents’ genes but also the family ecology and its social milieu. Thus, parenting skills, housing, neighborhood, schools, and other factors (eg, medical care) all have complex relations to each other and influence how each child’s genetic canvas is expressed. Accompanying this technical report is a policy statement that describes specific actions that pediatricians and other child advocates can take to attenuate the negative effects of the mediators identified in this technical report and improve the well-being of our nation’s children and their families.

La anemia en niños menores de tres años es un problema de salud pública en el Perú y el mundo. Se estima que la causa principal de la anemia, aunque no la única, es la deficiencia de hierro. Existen muchos estudios y revisiones sobre cómo esta carencia en los infantes impacta negativamente en el desarrollo psicomotor y, a pesar de corregirse la anemia, los niños con este antecedente presentan, a largo plazo, un menor desempeño en las áreas cognitiva, social y emocional. Estos hallazgos se describen en estudios observacionales, de seguimiento, así como en experimentales con grupo control. La anemia puede disminuir el desempeño escolar, y la productividad en la vida adulta, afectando la calidad de vida, y en general la economía de las personas afectadas. Se describen algunos posibles mecanismos de cómo la deficiencia de hierro, con o sin anemia, podría afectar el desarrollo en la infancia; por ello, causa preocupación la alta prevalencia de anemia que se observa en este grupo de edad. La prevención de la anemia en el primer año de vida debe ser la meta para evitar consecuencias en el desarrollo de la persona a largo plazo. / Anemia in children younger than 3 years is a public health problem in Peru and worldwide. It is believed that one of the primary causes of anemia is iron deficiency. Numerous studies and reviews have reported that iron deficiency limited psychomotor development in children and that, despite the correction of anemia, children with iron deficiency experienced poorer long-term performance in cognitive, social, and emotional functioning. These outcomes were reported in observational studies, follow-up studies, and experimental studies with a control group. Anemia can decrease school performance, productivity in adult life, quality of life, and the general income of affected individuals. Here we describe possible mechanisms underlying the effect of iron deficiency, with or without anemia, on childhood development. The high rate of anemia in this age group is a cause for concern. Moreover, anemia should be prevented in the first year of life to avoid long-term negative effects on individual development. / La investigación ha sido financiada por el Instituto Nacional de Salud de Perú. / Revisión por pares

[Truncated abstract] This thesis examines the health outcomes of women exposed to blue asbestos at Wittenoom, Western Australia. Blue asbestos was mined and milled from 1943 to 1966 by the Australian Blue Asbestos Company (ABA) at Wittenoom, 1,600km from Perth in the remote Pilbara region of Western Australia. The original work for this thesis is presented in six manuscripts, some of which have been published in peer-reviewed Journals. The following aims have been investigated. 1. (a) To compare the all-cause mortality rates of women who lived at Wittenoom compared with all-cause mortality rates of the Western Australian female population (b) To assess the exposure-response relationship between asbestos and mortality in women. 2. (a) To compare the incidence rates of common cancers in women who lived at Wittenoom, compared with the incidence rates of these cancers in the Western Australian female population. (b) To assess the exposure-response relationship between asbestos and cancer incidence at various sites in women. 3. (a) To determine if reproductive cancers (ovarian, uterine cervical and corpus and breast) and gestational trophoblastic diseases are associated with asbestos exposure. v (b) To determine if ovarian cancer has been misclassified as malignant peritoneal mesothelioma or vice versa. (c) To determine if colon cancer has been misclassified as malignant peritoneal mesothelioma or vice versa. (d) To assess the exposure-response relationship between asbestos and reproductive cancer incidence. 4. To assess the susceptibility of women to asbestos exposure in comparison with men with similar exposure histories. 5. To predict the future mortality from malignant mesothelioma among women who lived at Wittenoom. '...' The Wittenoom crocidolite industry has had a damaging impact upon the health of the women workers and residents who lived there. Wittenoom women are more likely to die from malignant mesothelioma and lung cancer, all cancers and all causes than women in the Western Australian population. This brief period of crocidolite mining in Western Australia's history will continue to exert a detrimental impact upon the future of the women who lived there, with another 66 to 87 mesotheliomas predicted to occur to the end of 2030.

No description available.

<p>The Swedish Cancer Register was used to determine the relative survival rate in colon and rectal cancer and to estimate the occurrence of second cancers related to radiation therapy for rectal cancer. The Swedish Hospital Discharge Register and hospital records were used to estimate the rate of late adverse effects due to radiation therapy for rectal cancer. The whole Swedish population was the source of the survival studies. Patients participating in the Uppsala Trial and the Swedish Rectal Cancer Trial on radiation therapy for rectal cancer constituted the subjects of the studies on late adverse effects and second cancers.</p><p>The main results of the survival analysis revealed a significant improvement in the 5-year relative survival rate for both colon and rectal cancer. During the time period 1960-1999, the survival improved from 39.6% to 57.2% in colon cancer and from 36.1% to 57.6% in rectal cancer.</p><p>Patients irradiated for rectal cancer, in addition to surgery, were at increased risk for a second cancer compared to those treated by surgery alone. This risk increase was mainly found for cancers developing in organs within or adjacent to the irradiated target (relative risk (RR) 2.04; 95% confidence interval (CI) 1.10–3.79). Furthermore, the most important late adverse effects of radiation therapy seem to be those on the gastrointestinal tract, in the form of small bowel obstruction (RR 1.88; 95%CI 1.10–3.20) and abdominal pain (RR 1.92; 95% CI 1.14–3.23). Overall, the benefit of radiation therapy was greater than its drawbacks, as a large reduction in local recurrences and better survival was noted in patients treated preoperatively with irradiation for rectal cancer.</p><p>In conclusion, significant improvements in the survival of patients with colon and rectal cancers have occurred in the last decades, especially in patients with rectal cancer. These improvements probably are related to advances in surgical and adjuvant treatment. The radiation therapy has several drawbacks, however, including an increased risk of second cancers and of bowel obstruction. This emphasises the need to further improve the radiation technique and to select only those patients for radiation therapy who are most likely to benefit from it.</p>

<p>The newly established Swedish Apheresis Registry makes it possible to do national inter-center comparisons. This study was undertaken to describe and analyze the use of therapeutic apheresis and the adverse effects in such therapy. The special case of plasma exchange as rescue therapy in multi-organ failure, including renal failure, was also studied. In Sweden, plasma for transfusion is prepared and stored to ensure rapid availability. Due to new EU legislation, validation of such plasma was performed. </p><p>The analysis indicated that the use of therapeutic apheresis was in line with recommendations of other international societies. The frequency and types of adverse effects were comparable to those reported in other studies from analogous time periods. Compared with other countries, it appears that more therapeutic resources are available in Sweden and that there is a lower frequency of adverse effects in specific procedures. No fatalities were reported. The unique comparison of differences between centers regarding plasma exchange identified areas for further improvement.</p><p>The study on plasma exchange as rescue therapy in severe sepsis or septic shock is the second largest reported. The result was promising, with a survival rate of 82%. The rapid availability of plasma for transfusion appears to be of clinical importance in patients with early coagulopathy and severe trauma but the present selection and storage procedures for plasma lead to a time-dependent increase of the number of units with cold-induced activation of the contact system and C1 inhibitor consumption before day 14. Improvements of plasma quality can be attained by using plasma from male donors only and by reducing the storage time from 14 to 7 days. </p><p>Further studies are needed to define the role of plasma exchange in severe sepsis/septic shock, to evaluate the outcome of each patient’s treatment and to establish the indications for the transfusion of plasma.</p>

No description available.