Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0243026 (sepsis)
 52,417 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The population decline of the nominate lesser black-backed gull Larus fuscus fuscus in the Gulf of Finland (northern Baltic) is caused by an exceedingly high chick mortality due to diseases. The chick diseases include degeneration in various internal organs (primarily liver), inflammations (mainly intestinal), and sepsis, the final cause of death. The hypothesis of starvation causing intestinal inflammations (leading to sepsis) was tested by attempting to reproduce lesions in apparently healthy herring gull L. argentatus chicks in captivity. The herring gull chicks were provided a similar low food-intake frequency as observed for the diseased chicks in the wild. However, empty alimentary tract per se did not induce the intestinal inflammations and therefore, inflammations seem to be innate or caused by other environmental factors in the diseased lesser black-backed chicks. They had very high concentrations of PCB in their liver; but the concentrations were not significantly higher than those of the healthy herring gull chicks, indicating a common exposure area for both species (i.e. the Baltic Sea). When compared to NOEL and LOEL values for TEQs in bird eggs our TEQ levels clearly exceed most or all of the values associated with effects. Compared with published data on fish-eating waterbirds, the DDE concentrations in the diseased lesser black-backed chicks were well above the levels previously correlated with decreased reproduction, while the residues in apparently healthy herring gulls were below those levels. The DDE/PCB ratio in lesser black-backs was significantly elevated, indicating an increased exposure to DDTs as compared with most other Baltic and circumpolar seabirds. The possible exposure areas of DDT in relation to differential migration habits of the two gull species are discussed.
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PMID:Organochlorine concentrations in diseased vs. healthy gull chicks from the northern Baltic. 1463 2

Hunger strike is described as voluntary refusal of food and/or fluids. Prolonged starvation may produce many adverse events including even death in rare circumstances. Here, we present three fatal cases (all males, 25-38 years) died from hunger strike. In all corpses, obvious muscle wasting with reduced subcutaneous and internal fat deposits, and atrophy in some organs were demonstrated at autopsy. The extraordinary long starvation period before death could presumably be linked to the thiamine uptake in this period, which had been discontinued by all subjects before the death occurred. Prolonged caloric deficiency with subsequent complications such as multiple organ failure, severe sepsis and ventricular fibrillation could account as major causes of death in these subjects. The competence of the physicians working with hunger strikers about the processes and potential problems is of great importance since they have to acknowledge about them to their patients.
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PMID:Deaths due to hunger strike: post-mortem findings. 1548 19

The purpose of this paper is to review clinical studies on hypophosphatemia in pediatric intensive care unit patients with a view to verifying prevalence and risk factors associated with this disorder. We searched the computerized bibliographic databases Medline, Embase, Cochrane Library, and LILACS to identify eligible studies. Search terms included critically ill, pediatric intensive care, trauma, sepsis, infectious diseases, malnutrition, inflammatory response, surgery, starvation, respiratory failure, diuretic, steroid, antiacid therapy, mechanical ventilation. The search period covered those clinical trials published from January 1990 to January 2004. Studies concerning endocrinological disorders, genetic syndromes, rickets, renal diseases, anorexia nervosa, alcohol abuse, and prematurity were not included in this review. Out of 27 studies retrieved, only 8 involved pediatric patients, and most of these were case reports. One clinical trial and one retrospective study were identified. The prevalence of hypophosphatemia exceeded 50%. The commonly associated factors in most patients with hypophosphatemia were refeeding syndrome, malnutrition, sepsis, trauma, and diuretic and steroid therapy. Given the high prevalence, clinical manifestations, and multiple risk factors, the early identification of this disorder in critically ill children is crucial for adequate replacement therapy and also to avoid complications.
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PMID:Hypophosphatemia in critically ill children. 1554 5

Maternal starvation is a significant cause of intrauterine growth restriction (IUGR) in the world and increases the risk of infection in the neonate. We examined the effect of maternal starvation on Toll like receptor (TLR)4 expression in hepatic, splenic and intestinal tissues obtained from the adult IUGR offspring of prenatal calorie restricted rats. The hepatic TLR4 protein concentration was undetectable in the IUGR rats that had restricted milk intake during the suckling period (SM/SP; n = 4. p < 0.05) as compared to the normal growth controls (CM/CP; n = 4), and access to ad lib milk intake during the sucking period partially corrected the hepatic TLR4 expression (SM/CP; n = 4). IUGR had no effect on the splenic (n = 4) or intestinal (n = 4) TLR4 mRNA levels. In the liver, IUGR led to a 20% increase in baseline tumor necrosis factor (TNF)-alpha mRNA expression (p < 0.03) and a 70% increase in interleukin-1beta (IL-1beta) mRNA expression (p < 0.008) as compared to the control rats (CM/CP; n = 7). LPS-induced hepatic TNF-alpha release was significantly higher in SM/SP as compared to CM/CP. We propose that IUGR dysregulates TLR4 expression and function in the offspring, which may help explain the increased risk of Gram-negative sepsis and inflammatory diseases in this population.
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PMID:Intra-uterine growth restriction downregulates the hepatic toll like receptor-4 expression and function. 1571

THE PREGNANT PATIENT: Age; maternal disease; prophylactic antibiotics; gastroesophageal reflux; obesity; starvation; genotyping; coagulopathy; infection; substance abuse; altered drug responses in pregnancy; physiological changes of pregnancy. THE FETUS: Fetal monitoring; intrauterine surgery. THE NEWBORN: Breastfeeding; maternal infection, fever, and neonatal sepsis evaluation. OBSTETRIC COMPLICATIONS: Embolic phenomena; hemorrhage; preeclampsia; preterm delivery. OBSTETRIC MANAGEMENT: External cephalic version and cervical cerclage; elective cesarean delivery; fetal malpresentation; vaginal birth after cesarean delivery; termination of pregnancy. OBSTETRIC ANESTHESIA: Analgesia for labor and delivery; anesthesia for cesarean delivery; anesthesia for short obstetric operations; complications of anesthesia. MISCELLANEOUS: Consent; ethics; history; labor support; websites/books/leaflets/journal announcements.
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PMID:What's new and novel in obstetric anesthesia? Contributions from the 2003 scientific literature. 1579 48

The aims of this study were to estimate the occurrence of hypophosphatemia and to identify potential risk factors and outcome measures associated with this disturbance in children admitted to a pediatric intensive care unit. Data concerning 42 children admitted consecutively to 1 pediatric intensive care unit over a 1-year period were examined. Serum phosphorus levels were measured on the third day of admission, where levels below 3.8 mg/dL were considered indicative of hypophosphatemia. Hypophosphatemia was found in 32 children (76%), and there was a significant association between this disturbance and malnutrition (P = .04). Of the potential risk factors such as sepsis, diuretic/steroid therapy, starvation (over 3 days), and Pediatric Index of Mortality, none discriminated for hypophosphatemia. There were no associations between hypophosphatemia and mortality, length of stay in the pediatric intensive care unit, or time on mechanical lung ventilation. Hypophosphatemia was a common finding in critically ill children and was associated with malnutrition.
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PMID:Hypophosphatemia in children hospitalized within an intensive care unit. 1685 58

The blood-brain barrier (BBB) prevents the unrestricted movement of peptides and proteins between the brain and blood. However, some peptides and regulatory proteins can cross the BBB by saturable and non-saturable mechanisms. Leptin and insulin each cross the BBB by their own transporters. Impaired transport of leptin occurs in obesity and accounts for peripheral resistance; that is, the condition wherein an obese animal loses weight when given leptin directly into the brain but not when given leptin peripherally. Leptin transport is also inhibited in starvation and by hypertriglyceridemia. Since hypertriglyceridemia occurs in both starvation and obesity, we have postulated that the peripheral resistance induced by hypertriglyceridemia may have evolved as an adaptive mechanism in response to starvation. Insulin transport is also regulated. For example, treatment of mice with lipopolysaccharide (LPS) increases insulin transport across the BBB by about threefold. Since many of the actions of CNS insulin oppose those of peripheral insulin and since LPS releases proinflammatory cytokines, enhanced transport of insulin across the BBB could be a mechanism which promotes insulin resistance in sepsis. The brain endothelial cells which comprise the BBB secrete many substances including cytokines. Such secretion can be stimulated from one side of the BBB with release into the other side. For example, it appears that adiponectin can inhibit release of interleukin-6 from brain endothelial cells. Overall, the BBB represents an important interface in mediating gut-brain axes.
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PMID:The blood-brain barrier as a regulatory interface in the gut-brain axes. 1690 39

Burn trauma is a clinical condition accompanied by muscle wasting that severely impedes rehabilitation in burn survivors. Mitochondrial uncoupling protein 3 (UCP3) is uniformly expressed in myoskeletal mitochondria and its expression has been found to increase in other clinical syndromes that, like burn trauma, are associated with muscle wasting (e.g., starvation, fasting, cancer, sepsis). The aim of this study was to explore the effects of burn trauma on UCP3 expression, intramyocellular lipids, and plasma-free fatty acids. Mice were studied at 6 h, 1 d and 3 d after nonlethal hindlimb burn trauma. Intramyocellular lipids in hindlimb skeletal muscle samples collected from burned and normal mice were measured using 1H NMR spectroscopy on a Bruker 14.1 Tesla spectrometer at 4 degrees C. UCP3 mRNA and protein levels were also measured in these samples. Plasma-free fatty acids were measured in burned and normal mice. Local burn trauma was found to result in: 1) upregulation of UCP3 mRNA and protein expression in hindlimb myoskeletal mitochondria by 6 h postburn; 2) increased intramyocellular lipids; and 3) increased plasma-free fatty acids. Our findings show that the increase in UCP3 after burn trauma may be linked to burn-induced alterations in lipid metabolism. Such a link could reveal novel insights into how processes related to energy metabolism are controlled in burn and suggest that induction of UCP3 by burn in skeletal muscle is protective by either activating cellular redox signaling and/or mitochondrial uncoupling.
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PMID:Uncoupling protein 3 expression and intramyocellular lipid accumulation by NMR following local burn trauma. 1708 30

Muscle damage with a lack of regeneration, manifests itself in several life-threatening diseases, including cancer cachexia, congestive heart failure, AIDS and sepsis. Often misdiagnosed as a condition simply of weight loss, cachexia is actually a highly complex metabolic disorder involving features of anorexia, anaemia, lipolysis and insulin resistance. A significant loss of lean body mass arises from such conditions, resulting in wasting of skeletal muscle. Unlike starvation, the weight loss seen in chronic illnesses arises equally from loss of muscle and of fat. The cachectic state is particularly problematic in cancer, typifying poor prognosis and often lowering responses to chemotherapy and radiation treatment. More than half of cancer patients suffer from cachexia, and strikingly, nearly one-third of cancer deaths are related to cachexia rather than the tumour burden. In considering this disorder, we are faced with a conundrum; how is it possible for uncontrolled growth to prevail in the tumour, in the face of unrestrained tissue loss in our muscles? Consistently, the catabolic state has been associated with a shift in the homeostatic balance between muscle synthesis and degradation mediated by the actions of growth factors and cytokines. Indeed, tumour necrosis factor-alpha (TNF-alpha) levels are raised in several animal models of cachectic muscle wasting, whereas the insulin-like growth factor (IGF) system acts potently to regulate muscle development, hypertrophy and maintenance. This concept of skeletal muscle homeostasis, often viewed as the net balance between two separate processes of protein synthesis and degradation has however changed. More recently, the view is that these two biochemical processes are not occurring independently of each other but in fact are finely co-ordinated by a web of intricate signalling networks. This review, therefore, aims to discuss data currently available regarding the mechanisms of degeneration and regeneration with specific emphasis on the potential and controversial cross-talk which may exist between anabolic growth factors (e.g. IGF-I) and catabolic cytokines (e.g. TNF-alpha). Also importantly, the potential impact at a cellular level of exercise, diet and age will be addressed. Finally, the ability to 'hi-jack' signalling pathways traditionally believed to be for growth and survival or death will be reviewed. It is anticipated that such a review will highlight significant gaps in our knowledge of the cachectic state as well as provide caution with regards to therapeutics suggesting total block on inflammatory processes such as that associated with TNF-alpha action.
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PMID:Waste management - cytokines, growth factors and cachexia. 1711 96

The small intestine acts as interface and regulator between the gut lumen and the rest of the body and controls the degree and rate of transport of amino acids coming from dietary protein via the portal vein to the liver and the systemic circulation. To measure protein absorption, kinetics multicatheter animal (pig) models in combination with amino acid tracer technology are available. Dietary factors influence the absorption rates from the lumen to the gut, metabolism of dietary component in the gut, and the release of amino acids to the portal circulation from digested protein. In a balanced-protein meal, the gut dietary amino acid utilization (30-50%) for gut protein synthesis will result in a labile protein pool in the gut that can be beneficial during the postabsorptive state. To enhance gut retention, amount and quality of protein and the presence of carbohydrate are major factors. Besides this the use of a slowly digestible protein or the presence of fiber in the meal can increase retention further. During the absorption of low-quality protein meals, fewer amino acids are utilized by the gut, resulting in higher amounts of amino acid release to the portal circulation. Malnutrition or starvation, protein depletion, deficiencies of specific nutrients, or illness such as sepsis all inhibit the growth and change protein turnover of the intestinal mucosa and therefore affect absorption kinetics. Therefore, the kind of protein meal that has the most optimal absorption kinetics (the most beneficial) for gut and for the rest of the body depends on these (patho)physiological circumstances. Despite the absence of different absorption kinetics between protein, peptides, and amino acids, they could be beneficial in specific circumstances.
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PMID:Absorption kinetics of amino acids, peptides, and intact proteins. 1857 72


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