bluuebunny/crossref_metadata_2025_split huggingface dataset:
Nutrition support in major burn injury: case analysis of dietetic activity, resource use and cost implications
Authors: Windle E. M. 
Published: March 2008

AbstractBackground  Patients with major burn injury are among the most catabolic and nutritionally vulnerable of all hospital admissions. A considerable amount of dietetic intervention is often required. To date, UK practice has not been described in detail. This study aimed to identify nutritional interventions, resource use and associated costs for a typical patient admitted with major burns.Methods  A 28‐year‐old male with 43.5% total body surface area flame injury was selected for study. Dietetic, medical and pharmacy records were reviewed for data regarding nutritional status, interventions and product use. Costs of dietetic staffing, nutrition support products, related ancillary items and hospital food provision were calculated.Results  The patient required 68 days of nutrition support, including 40 days of nasogastric tube feeding. Seventy per cent of bedside reviews resulted in dietetic intervention. Initiation of nutrition support, substrate use, and frequency of biochemical and weight monitoring were largely in compliance with practice guidelines. Overall cost of nutritional care for the inpatient episode was £1377.Conclusion  Work is now required to assess current nutrition practices across different UK centres and for a range of burn severities, to establish a baseline from which resource and financial requirements can ultimately be developed.
Three persons with multiple disabilities accessing environmental stimuli and asking for social contact through microswitch and VOCA technology
Authors: Lancioni G. E. , O'Reilly M. F. , Singh N. N. , Sigafoos J. , Oliva D. , Severini L. 
Published: March 2008

AbstractBackground  Direct access to environmental stimuli and opportunity to ask for social contact/attention may be considered highly relevant objectives for persons with multiple disabilities. We assessed the possibility of enabling three of these persons (two children and one adolescent) to combine two microswitches (for accessing environmental stimuli) and a Voice Output Communication Aid (VOCA), which allowed them to ask for caregiver's attention.Methods  Initially, the participants were required to use each of the two microswitches individually and then together. Thereafter, they were taught to use the VOCA. Eventually, the VOCA was available together with the microswitches, and the participants could use any of the three.Results  The results, which support preliminary data on this topic, showed that all participants (1) were able to operate the two microswitches as well as the VOCA; and (2) used all three of them consistently when they were simultaneously available.Conclusions  Teaching persons with multiple disabilities to combine a VOCA with conventional microswitches may enrich their general input, emphasize their active social role and eventually enhance their social image.
Behavioural characteristics associated with dementia assessment referrals in adults with Down syndrome
Authors: Adams D. , Oliver C. , Kalsy S. , Peters S. , Broquard M. , Basra T. , Konstandinidi E. , McQuillan S. 
Published: March 2008

AbstractBackground  Behavioural changes associated with dementia in Down syndrome are well documented, yet little is known about the effect of such behaviours on carers and referral. By comparing the behavioural and cognitive profiles of individuals referred for a dementia assessment with those of individuals not referred, some insight can be gained into behavioural characteristics that initiate referral for specialist support or interventions.Method  Forty‐six adults with Down syndrome were divided into two groups dependent upon method of entry into the study; post‐referral to a specialist service for older adults with intellectual disabilities and Down syndrome for a dementia assessment (n = 17) or after receiving information sent out to day centres and residential homes (n = 29). These groups were compared on established measures of dementia alongside two informant measures of behaviour.Results  Those referred for a dementia assessment evidenced scores indicative of cognitive decline on both informant and direct Neuropsychological Assessments and showed more behavioural excesses, but not deficits, and lower socialisation and coping skills than those in the comparison group. Carers of those referred for a dementia assessment reported a greater impact of behavioural excesses on staff than on the individual showing the behaviour in contrast to the comparison group.Conclusion  The behavioural differences between those referred and the comparison group suggest that two factors are involved in the instigation of a referral for a dementia assessment: the nature of the behavioural presentation (excesses rather than deficits) and the effect of that behavioural change upon the care staff.
Nitric oxide synthesis and signalling in plants
Authors: WILSON IAN D. , NEILL STEVEN J. , HANCOCK JOHN T. 
Published: March 2008

ABSTRACTAs with all organisms, plants must respond to a plethora of external environmental cues. Individual plant cells must also perceive and respond to a wide range of internal signals. It is now well‐accepted that nitric oxide (NO) is a component of the repertoire of signals that a plant uses to both thrive and survive. Recent experimental data have shown, or at least implicated, the involvement of NO in reproductive processes, control of development and in the regulation of physiological responses such as stomatal closure. However, although studies concerning NO synthesis and signalling in animals are well‐advanced, in plants there are still fundamental questions concerning how NO is produced and used that need to be answered. For example, there is a range of potential NO‐generating enzymes in plants, but no obvious plant nitric oxide synthase (NOS) homolog has yet been identified. Some studies have shown the importance of NOS‐like enzymes in mediating NO responses in plants, while other studies suggest that the enzyme nitrate reductase (NR) is more important. Still, more published work suggests the involvement of completely different enzymes in plant NO synthesis. Similarly, it is not always clear how NO mediates its responses. Although it appears that in plants, as in animals, NO can lead to an increase in the signal cGMP which leads to altered ion channel activity and gene expression, it is not understood how this actually occurs.NO is a relatively reactive compound, and it is not always easy to study. Furthermore, its biological activity needs to be considered in conjunction with that of other compounds such as reactive oxygen species (ROS) which can have a profound effect on both its accumulation and function. In this paper, we will review the present understanding of how NO is produced in plants, how it is removed when its signal is no longer required and how it may be both perceived and acted upon.
Transfusion support for a patient with McLeod phenotype without chronic granulomatous disease and with antibodies to Kx and Km
Authors: Bansal I. , Jeon H.‐R. , Hui S. R. , Calhoun B. W. , Manning D. W. , Kelly T. J. , Lee S. , Baron B. W. 
Published: March 2008

Background and Objectives  Kell antigens are encoded by the KEL gene on the long arm of chromosome 7. Kx antigen is encoded by the XK gene on the short arm of the X chromosome. Kell and Kx proteins in the red cell membrane are covalently linked by a disulphide bond. The McLeod phenotype is characterized by weakened expression of antigens in the Kell blood group system, absence of Km and Kx antigens, and acanthocytosis. It has an X‐linked mode of inheritance with transmission through carrier females. Some males with the McLeod syndrome also have chronic granulomatous disease (CGD). It is generally believed that patients with non‐CGD McLeod may develop anti‐Km but not anti‐Kx, but that those with CGD McLeod can develop both anti‐Km and anti‐Kx.Materials and Methods  We present serological data, DNA genotyping and gene sequencing, monocyte monolayer assay and neutrophil oxidative burst test from a patient with the McLeod phenotype without clinical evidence of CGD.Results  We report here the second example of a patient with non‐CGD McLeod who developed anti‐Kx in addition to anti‐Km. Sequencing of our patient's XK gene confirmed the presence of a mutation resulting in a premature stop codon and lack of Kx protein in the red cell membrane, which is consistent with the diagnosis of McLeod syndrome. Neutrophil oxidative burst test was normal, indicating that our patient did not have CGD. The challenge of providing 10 compatible blood units for multiple surgeries was met.Conclusion  The second case of a rare entity, a patient with non‐CGD McLeod who developed anti‐Kx and anti‐Km, was managed successfully with a combination of autologous donations and procurement of compatible units from national and international sources.
Efficacy and tolerability of human fibrinogen concentrate administration to patients with acquired fibrinogen deficiency and active or in high‐risk severe bleeding
Authors: Danés A. Farriols , Cuenca L. Gallur , Bueno S. Rodríguez , Mendarte Barrenechea L. , Ronsano J. Bruno Montoro 
Published: March 2008

Background and Objectives  Fibrinogen deficiency is a cause for massive haemorrhage whose management in emergency situations is the subject of debate. Plasma‐derived fibrinogen concentrates are indicated for reversing the haemorrhagic diathesis found in congenital and acquired deficiencies.Materials and Methods  We report on the results of an observational study that evaluated the effects of fibrinogen concentrates in patients suffering from various forms of acquired severe hypofibrinogenaemia with life‐threatening consumptive thrombo‐haemorrhagic disorders (surgery, trauma and digestive haemorrhage), or underlying disease states that limit fibrinogen synthesis (hepatic dysfunction, haematological malignancies).Results  Sixty‐nine patients were identified and included, in whom most of the processes (62%) corresponded to consumptive hypofibrinogenaemia. After a median dose of 4 g, a mean absolute increase of 1·09 g/l in plasma fibrinogen was measured and coagulation parameters were significantly improved (P < 0·001). Mortality rates of 32·3% and 44·2% were reported after 24 h and 72 h, respectively.Conclusion  We conclude that the administration of fibrinogen concentrates in unresponsive, life‐threatening haemorrhage with acquired hypofibrinogenaemia improves laboratory measures of coagulation, and may also be life saving. Although observational in nature, our data indicate a direct relationship between plasma fibrinogen levels and survival in acquired fibrinogen deficiency. Further studies are warranted to ascertain a clear relationship between fibrinogen levels and survival.
Mitochondrial mechanisms of death responses in pancreatitis
Authors: Odinokova Irina V , Sung Kai‐Feng , Mareninova Olga A , Hermann Kip , Gukovsky Ilya , Gukovskaya Anna S 
Published: March 2008

AbstractPancreatitis is a severe and frequently lethal disorder, a major cause of which is alcohol abuse. Parenchymal cell death is a major complication of pancreatitis. In experimental models of acute pancreatitis, acinar cells have been shown to die through both necrosis and apoptosis, the two principal pathways of cell death. The severity of experimental acute pancreatitis correlates directly with the extent of necrosis and inversely with apoptosis. Thus, understanding the regulation of apoptosis and necrosis is becoming exceedingly important in investigations of the pathogenesis and treatment of pancreatitis. Over the past decade, the mitochondria have emerged as a master regulator of cell death in various physiological and pathological processes. Release of mitochondrial cytochrome c into the cytosol is a central event in apoptosis, whereas mitochondrial depolarization resulting in ATP depletion leads to necrosis. The present review focuses on the mitochondrial mechanisms of death responses in pancreatitis, with emphasis on mitochondrial membrane permeabilization and its role in the balance between apoptosis and necrosis in acute pancreatitis, and alcohol's effects on death responses of pancreatitis.
Impaired receptor‐mediated endocytosis: Its role in alcohol‐induced apoptosis
Authors: Casey Carol A , Lee Serene ML , Aziz‐Seible Razia , McVicker Benita L 
Published: March 2008

AbstractHepatocyte apoptosis, inflammation, and fibrosis are prominent features of liver disease in general and of alcoholic liver injury in particular. Although the link between these processes remains unclear, one universal characteristic of liver injury is the induction of hepatocellular damage, which results in the generation of apoptotic bodies. Work from our laboratory over the last several years has studied the effect of ethanol administration on the process of apoptosis and a role for altered endocytosis in alcoholic apoptosis. We initially focused our research on the hepatocyte by examining endocytosis using the asialoglycoprotein receptor (ASGP‐R) pathway as a model and we identified multiple ethanol‐induced impairments in receptor function. We also showed that uptake of apoptotic bodies is impaired in hepatocytes isolated from ethanol‐fed animals compared to controls, and that this impairment is linked to altered ASGP‐R function. Recent work from our laboratory is examining a link between ethanol‐impaired ASGP‐R function, apoptotic body accumulation, and inflammation in the liver. We are particularly interested in data showing that factors produced by Kupffer cells incubated with apoptotic bodies can lead to production of tumor necrosis factor‐alpha and interleukin‐6, and that this effect is exacerbated in the setting of alcohol administration. In addition, we have preliminary data showing that media from Kupffer cell cultures incubated with apoptotic bodies can induce hepatocyte killing. The goal of our future work is to show that inadequate removal of apoptotic cells, in part via altered receptor‐mediated endocytosis, plays a role in the course of pathogenesis of alcoholic liver injury.
Oxidative stress in alcoholic liver disease: Role of NADPH oxidase complex
Authors: De Minicis Samuele , Brenner David A 
Published: March 2008

AbstractAlcohol is a well‐known risk factor for liver damage and is one of the major causes of liver disease worldwide. Chronic intake of alcohol, over a certain limit, inevitably leads to hepatic steatosis. If the injury persists, steatosis with concomitant tumor necrosis factor‐α and other cytokines, progresses to steatohepatitis, fibrosis and finally cirrhosis. Among the multiple factors involved in the process of alcohol‐induced liver injury, a crucial role is played by oxidative stress. Several mechanisms during ethanol metabolism result in reactive oxygen species (ROS) production. Although the main site of ethanol metabolism is hepatocytes, other mechanisms are involved in alcohol‐induced liver injury. Specifically, in the ROS production activity, an important role is played by the NADPH oxidase complex. NADPH oxidase is expressed in hepatocytes, hepatic stellate cells and Kupffer cells in the liver. Studying NADPH oxidase gives new insights into alcohol‐induced liver damage and provides new direction for future therapeutic strategies.
Association analysis among polymorphisms of the various genes and chronic alcoholic pancreatitis
Authors: Maruyama Katsuya , Harada Shoji , Yokoyama Akira , Naruse Satoru , Hirota Masahiko , Nishimori Isao , Otsuki Makoto 
Published: March 2008

AbstractChronic and excessive consumption of alcohol is an important factor responsible for the onset of pancreatitis. However, the incidence of chronic pancreatitis in heavy drinkers differs in individuals, suggesting that these individual differences may involve various genetic and environmental factors. In the present study, we investigated an association of alcoholic pancreatitis with polymorphisms of the various genes related to metabolism of the oxidative compounds. We analyzed polymorphisms of NADPH‐quinone oxidoreductase 2 (NQO2), multidrug resistance 1 (MDR1), alcohol dehydrogenase 1B (ADH1B) and lipoprotein lipase (LPL). The subjects consisted of 53 patients with chronic alcoholic pancreatitis (AlCP), 54 alcoholic patients without pancreatic dysfunction (Alc), and 42 healthy individuals. DNA samples were prepared from the peripheral blood of all subjects, and the genetic mutations were analyzed by polymerase chain reaction and restriction fragment length polymorphism methods. The ADH1B gene frequencies were significantly different between healthy controls and Alc patients (P < 0.001), and also between AlCP and Alc patients (P < 0.05). However, no significant difference was found between healthy controls and AlCP patients. The gene frequencies of MDR1 (3435C > T) and MDR1 (2677G > A/T) of patients with AlCP or Alc were different when compared with healthy controls, although the difference was not significant. The NQO2 and LPL genes showed no relation with Alc and AlCP patients. The ADH1B*1 gene frequency in AlCP was significantly lower compared with Alc. We speculate that the ADH1B*1 gene may function by reducing vulnerability to the onset of alcoholic pancreatitis. Other genes analyzed in the present study lacked association with AlCP.
Molecular basis for the synergy between alcohol and hepatitis C virus in hepatocarcinogenesis
Authors: Koike Kazuhiko , Tsutsumi Takeya , Miyoshi Hideyuki , Shinzawa Seiko , Shintani Yoshizumi , Fujie Hajime , Yotsuyanagi Hiroshi , Moriya Kyoji 
Published: March 2008

AbstractOverwhelming lines of epidemiological evidence have indicated that persistent infection with hepatitis C virus (HCV) is a major risk for the development of hepatocellular carcinoma (HCC). In addition, heavy alcohol use has been linked with earlier progression to HCC in chronic hepatitis C patients. However, in the pathogenesis of HCV‐associated HCC, it still remains controversial as to whether the virus plays a direct or an indirect role, and as to how alcohol operates in the acceleration of HCC development. Several studies using transgenic mouse models, in which the core protein of HCV has an oncogenic potential, indicate that HCV is directly involved in hepatocarcinogenesis, although other factors such as continuous inflammation or environmental factors seem also to play a role. The downstream events of the HCV core protein expression in the transgenic mouse HCC model are segregated into two pathways. One is the augmented production of oxidative stress in the absence of inflammation along with the attenuation of some scavenging systems in the putative preneoplastic stage with steatosis in the liver. The other pathway is the alteration in cellular gene expression and intracellular signaling, including the mitogen‐activated protein kinase cascade. The combination of these pathways would explain the unusually high incidence and multicentric nature of HCC development in HCV infection. In addition, alcohol feeding in this animal model further activated the two pathways synergistically with HCV, leading to an earlier development of HCC. Such a synergy would reveal the molecular basis for the acceleration of HCC development by alcohol in HCV infection.
Alcohol, cofactors and the genetics of hepatocellular carcinoma
Authors: Yu Mimi C , Yuan Jian‐Min , Lu Shelly C 
Published: March 2008

AbstractHeavy alcohol consumption, chronic infection with the hepatitis B virus (HBV) or the hepatitis C virus (HCV), tobacco smoking, and diabetes are risk factors for hepatocellular carcinoma (HCC). In the Los Angeles Non‐Asian HCC Study, heavy alcohol intake was shown to exhibit synergistic effects with viral hepatitis (HBV, HCV) and diabetes in the causation of HCC among individuals with joint exposures. Although chronic infection with HBV is recognized as the most important causal factor for HCC in humans, only a minority of HBV carriers eventually develop HCC, suggesting the presence of important cofactors in HBV‐related HCC. In the Guangxi/China HCC Study, a 20‐fold difference in HCC risk was observed between individuals possessing the least versus the most favorable cytokine genotypes for hepatitis B viral clearance. Experimental studies have indicated an important role for one‐carbon metabolism in HCC development. In both the Los Angeles and Guangxi studies, low‐activity genotypes (reduced enzymatic activities) of methylenetetrahydrofolate reductase (MTHFR) and high‐activity genotypes (enhanced enzymatic activities) of thymidylate synthase (TYMS), both of which discourage the misincorporation of uracil into DNA, were shown to be associated with a reduced risk for HCC.
The longitudinal relationship between the systemic inflammatory response, circulating T‐lymphocytes, interleukin‐6 and ‐10 in patients undergoing immunotherapy for metastatic renal cancer
Authors: Ramsey Sara , Aitchison Michael , Graham John , McMillan Donald C. 
Published: March 2008

OBJECTIVETo examine the longitudinal relationship between the systemic inflammatory response, circulating T‐lymphocyte subpopulations, interleukin‐6 and ‐10 in patients undergoing immunotherapy for metastatic renal cancer, as the inflammation‐based Glasgow Prognostic Score (GPS) provides additional prognostic information in patients with advanced renal cancer, but the basis of the relationship between the systemic inflammatory response and poorer survival is not clear, and nor is the effect of immunotherapy on related variables.PATIENTS AND METHODSThe study included 23 patients with metastatic renal cancer and starting immunotherapy. Samples of blood were drawn for routine laboratory analysis and to quantify cytokines using enzyme‐linked immunosorbent assays before immunotherapy, and repeated after 2 weeks of treatment.RESULTSMost patients had a good performance status, favourable or intermediate Memorial Sloane‐Kettering Cancer Center (MSKCC) risk scores, and with elevated C‐reactive protein (>10 mg/L), GPS (1 or 2), interleukin‐6 (>4 pg/mL) and interleukin‐10 (>10 pg/mL). Patients who completed one cycle of immunotherapy were more likely to have a normal MSKCC (P < 0.05) or GPS (P < 0.05) scores, whilst the percentage of lymphocytes was lower (P < 0.05). The MSKCC and the GPS scores did not alter significantly during one cycle of immunotherapy. Similarly, leukocyte counts, CD4+ and CD8+ T‐lymphocytes, interleukin‐6 and ‐10 concentrations did not change significantly.CONCLUSIONSThe pretreatment systemic inflammatory response and its related lymphopenia are important in determining the tolerance to immunotherapy in patients with metastatic renal cancer. Immunotherapy is not associated with changes in circulating T‐lymphocytes, nor the systemic inflammatory response.