Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036690 (sepsis)
 59,461 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

During tumor growth, anorexia and reduced food intake markedly contribute to the development of malnutrition, thus worsening overall patients' survival. A better understanding of the pathophysiology of eating behavior may lead to new and more effective therapies, aiming at counteracting the detrimental effects of anorexia and reduced food intake on nutritional status and survival in cancer patients. Brain tryptophan and serotonin concentrations seem to play a pivotal role in the regulation of eating behavior. Increased brain serotonin activity is indeed associated with a reduction of food intake. It has been recently hypothesized that increased availability of tryptophan to the brain and the consequent increased serotonin activity may represent the pathogenic mechanism for cancer-associated anorexia. According to this hypothesis, the modulation of brain serotonin activity may result in an improvement of anorexia. Reducing brain tryptophan availability represents a possible mechanism to restore brain serotonin activity to normal. There is evidence that the oral administration of neutral amino acids competing with tryptophan for brain entry results in a significant improvement of cancer anorexia. The same treatment may also be effective in improving secondary anorexia, which is associated with other chronic illnesses, including renal and liver failure, sepsis, and so forth, sharing a similar pathogenic mechanism.
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PMID:Cancer anorexia: new pathogenic and therapeutic insights. 885 Feb 21

Over the last years numerous studies have focussed on the in vivo expression of tissue factor (TF) in health and disease. The selective perivascular distribution of TF and the lethal effects of TF knockouts have added strong support to the widely accepted view that TF plays a pivotal role in the initiation of blood coagulation during physiological hemostasis. Inappropriate in vivo expression of TF, particularly by cells that do not express this protein under normal conditions (mainly monocyte-macrophages and endothelial cells), has been documented and is likely responsible for fibrin deposition in a variety of pathological conditions, among which sepsis-associated disseminated intravascular coagulation (DIC) and thromboembolic disease. In malignancy, in vivo expression of TF by tumor cells and/or by host cells has been implicated not only in intratumoral and systemic activation of blood coagulation but also in tumor growth and dissemination.
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PMID:Tissue factor in health and disease. 919 52

Hyaluronan (HA) is a high molecular weight polysaccharide present in the extracellular matrix of most tissues. It is a major component of loose connective tissues such as skin, synovial fluid and the vitreous body, and during embryonic development, tissue repair, tumor growth and at inflammatory sites. Increased serum concentrations have been reported in association with tissue damage, certain inflammatory diseases, notably rheumatoid arthritis and scleroderma, liver malfunction and in some malignancies. Currently there are no serological markers available that monitor the extent of tissue damage in vasculitis. We therefore, conducted this study to investigate the significance of serum HA in patient with systemic vasculitis (SV). Ten patients with SV and acute renal failure had elevated HA levels compared to normal age and gender matched controls (n = 31) (mean +/- SD: 673.8 +/- 495.14 micrograms/l and 90.26 +/- 37.18 micrograms/l, respectively; p < 0.001]. Eight of these patients were studied longitudinally for ten days, after pulse steroids, during which serum HA levels fell paralleling clinical improvement, despite the persistence of positive perinuclear-anti-neutrophil cytoplasmic antibody (p-ANCA) serology in three patients. In two patients, the clinical course was complicated by sepsis which was accompanied by an acute rise in serum HA. One patient suffered a relapse of vasculitis, with lung hemorrhage and a sudden rise in HA (> 2,000 micrograms/l), but c-ANCA serology remained normal. Serum HA was also measured in a further ten patients in clinical remission from SV and found to be within the normal range (82.44 +/- 39.06 micrograms/l). One patient, with equivocal clinical relapse after transplantation, exhibited high p-ANCA (404 IU) but serum HA remained normal (ten readings over six months 0-163 micrograms/l). Little change was seen in symptoms, or HA and ANCA serology, following plasma exchange. These preliminary data indicate that serum HA is raised in active vasculitis and may be a useful adjunctive marker of disease activity and extent of tissue damage.
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PMID:Serum hyaluronan levels follow disease activity in vasculitis. 924 72

Initially, total parenteral nutrition (TPN) was not used in cancer patients because of the fear of sepsis and the potential for stimulation of tumor growth. It was used first in cancer patients who had failed all attempts at enteral nutrition and in whom adequate anticancer therapy would have been otherwise impossible. TPN candidates today remain patients with responsive tumors who cannot tolerate the toxicity of cancer therapy because they are malnourished.
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PMID:Historical perspective on nutritional support of cancer patients. 952 22

In order to perform resections of tumors at critical sites in the liver in young children, liver resections in cardiac arrest and deep hypothermia under cardiopulmonary bypass have been developed. We report our experience with liver resection under cardiopulmonary bypass in three children with hepatoblastoma. In the first child the operation was performed under cardiac arrest and, the other two children were operated on under "low flow" conditions. The periods under cardiopulmonary bypass circulation were well tolerated. Extended right liver resections with vascular reconstructions were performed. The postoperative increase of liver enzymes was moderate. The increase in GOT was between 100 and 200 U/l. In spite of the extended tumor growth, reasonable long-term results were achieved by resection in combination with chemotherapy. One child has been living 8 years and another 10 months without tumor recurrence. The third child died due to sepsis during adjuvant chemotherapy, after she had recovered well from liver resection.
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PMID:[Extended liver resection in small children under circulatory arrest and "low-flow" cardiopulmonary bypass]. 1094 36

The brain and the immune system are the two major adaptive systems of the body. During an immune response the brain and the immune system "talk to each other" and this process is essential for maintaining homeostasis. Two major pathway systems are involved in this cross-talk: the hypothalamic-pituitary-adrenal (HPA) axis and the sympathetic nervous system (SNS). This overview focuses on the role of SNS in neuroimmune interactions, an area that has received much less attention than the role of HPA axis. Evidence accumulated over the last 20 years suggests that norepinephrine (NE) fulfills the criteria for neurotransmitter/neuromodulator in lymphoid organs. Thus, primary and secondary lymphoid organs receive extensive sympathetic/noradrenergic innervation. Under stimulation, NE is released from the sympathetic nerve terminals in these organs, and the target immune cells express adrenoreceptors. Through stimulation of these receptors, locally released NE, or circulating catecholamines such as epinephrine, affect lymphocyte traffic, circulation, and proliferation, and modulate cytokine production and the functional activity of different lymphoid cells. Although there exists substantial sympathetic innervation in the bone marrow, and particularly in the thymus and mucosal tissues, our knowledge about the effect of the sympathetic neural input on hematopoiesis, thymocyte development, and mucosal immunity is extremely modest. In addition, recent evidence is discussed that NE and epinephrine, through stimulation of the beta(2)-adrenoreceptor-cAMP-protein kinase A pathway, inhibit the production of type 1/proinflammatory cytokines, such as interleukin (IL-12), tumor necrosis factor-alpha, and interferon-gamma by antigen-presenting cells and T helper (Th) 1 cells, whereas they stimulate the production of type 2/anti-inflammatory cytokines such as IL-10 and transforming growth factor-beta. Through this mechanism, systemically, endogenous catecholamines may cause a selective suppression of Th1 responses and cellular immunity, and a Th2 shift toward dominance of humoral immunity. On the other hand, in certain local responses, and under certain conditions, catecholamines may actually boost regional immune responses, through induction of IL-1, tumor necrosis factor-alpha, and primarily IL-8 production. Thus, the activation of SNS during an immune response might be aimed to localize the inflammatory response, through induction of neutrophil accumulation and stimulation of more specific humoral immune responses, although systemically it may suppress Th1 responses, and, thus protect the organism from the detrimental effects of proinflammatory cytokines and other products of activated macrophages. The above-mentioned immunomodulatory effects of catecholamines and the role of SNS are also discussed in the context of their clinical implication in certain infections, major injury and sepsis, autoimmunity, chronic pain and fatigue syndromes, and tumor growth. Finally, the pharmacological manipulation of the sympathetic-immune interface is reviewed with focus on new therapeutic strategies using selective alpha(2)- and beta(2)-adrenoreceptor agonists and antagonists and inhibitors of phosphodiesterase type IV in the treatment of experimental models of autoimmune diseases, fibromyalgia, and chronic fatigue syndrome.
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PMID:The sympathetic nerve--an integrative interface between two supersystems: the brain and the immune system. 1112 11

A term female newborn was noted to have a tumor mass in the oral cavity soon after birth. Oral computer tomography revealed a well-enhanced soft tissue mass about 4 x 4 x 3 cm in size in the left buccal area. Group III embryonal type congenital rhabdomyosarcoma was diagnosed after biopsy (gross removal was not feasible). Respiratory distress exacerbated due to rapid tumor growth compressing airway with the result that endotracheal tube had to be intubated. Chemotherapy was done and complicated by two episodes of neutropenic fever and sepsis. Radiotherapy was suggested but refused by the family. Tumor size was slightly reduced and endotracheal tube could be removed four months later. She was taken home under regular chemotherapy. Radiotherapy, was, however, clearly indicated.
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PMID:Congenital rhabdomyosarcoma--a case report. 1139 4

A case of cardiac myxoma with multiple brain hemorrhage is reported. A 57-year-old male had complained of lower abdominal pain, diarrhea and fever for 3 days. On admission, he was in a condition of disseminated intravascular coagulation and sepsis. An abdominal CT scan showed infarction in the right kidney and spleen and an echocardiogram also showed myxoma in the left atrium. Although he presented no neurological symptoms, the brain CT showed multiple brain hemorrhage in the bilateral brain hemispheres. Total resection of the tumor was carried out for the improvement of the patient's general condition. Vimentin, S-100 protein and neuron specific enolase was positive in immunological staining and the pathological diagnosis was myxoma. Postoperative recovery of consciousness was poor and left hemiparesis developed. CT showed the increase of hematoma but angiography showed no cerebral aneurysm. The symptoms improved with conservative therapy. However the enhanced lesion remained in the right parietal lobe and an operation was performed 5 months later. The myxoma cell could not be found in the pathological examination, so tumor embolism, cerebral infarction, hemorrhagic infarction due to DIC, hematoma enlargement caused by heparinization during operation were suspected to have occurred in this order without tumor growth.
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PMID:[A case of cardiac myxoma with multiple brain hemorrhage]. 1145 99

Group B streptococcus (GBS) isolated from human neonates diagnosed with sepsis and respiratory distress produces a polysaccharide exotoxin (CM101) which has been previously described as GBS toxin. CM101 infused i.v. into tumor-bearing mice causes rapid tumor neovascularitis, infiltration of inflammatory cells, inhibition of tumor growth and tumor apoptosis. CM101 has successfully completed phase I studies in refractory cancer patients with very encouraging results. We have now demonstrated a mechanism of action for CM101. Using a normal mouse tumor model, we have examined tumor and normal tissues which were harvested at 0, 5, 15, 30 and 60min post-infusion of either CM101 or dextran. We present evidence that CM101 is rapidly (within the first 5min) bound to the tumor neovasculature. Complement is activated by the alternative pathway (C3) and leukocytes start to infiltrate the tumor within the first 5min. Through RT-PCR and immunohistochemical techniques, we demonstrate that proinflammatory cytokines, interleukin-6 and tumor necrosis factor (TNF)-alpha, are up-regulated in infiltrating leukocytes and TNF receptor 2 is up- regulated in the targeted tumor neovasculature. Combined, these events constitute possible explanations for the observed pathophysiology of tumor ablation.
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PMID:Functional studies on the anti-pathoangiogenic properties of CM101. 1451 62

Tissue factor (also known as tissue thromboplastin or CD142) is the protein that activates the blood clotting system by binding to, and activating, the plasma serine protease, factor VIIa, following vascular injury. Because of its essential role in hemostasis, tissue factor plays a role in pathology associated with hemostasis, triggering the coagulation system in many thrombotic diseases and the coagulopathies associated with sepsis and other forms of disseminated intravascular coagulation. Recent research has also implicated tissue factor in a variety of nonhemostatic roles, including cell signaling, inflammation, vasculogenesis, and tumor growth and metastasis. This review focuses on both the well-known roles of tissue factor in hemostasis and thrombosis and the newer concepts of tissue-factor biology including how it functions as a signaling receptor and the possible role of blood-borne tissue factor in thrombosis.
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PMID:Tissue factor: a key molecule in hemostatic and nonhemostatic systems. 1500 35


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