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71.
Skinner J Mee TJ Blackwell RP Maslanyj MP Simpson J Allen SG Day NE Cheng KK Gilman E Williams D Cartwright R Craft A Birch JM Eden OB McKinney PA Deacon J Peto J Beral V Roman E Elwood P Alexander FE Mott M Chilvers CE Muir K Doll R Taylor CM Greaves M Goodhead D Fry FA Adams G Law G;United Kingdom Childhood Cancer Study Investigators 《British journal of cancer》2002,87(11):1257-1266
The United Kingdom Childhood Cancer Study, a population-based case-control study covering the whole of Great Britain, incorporated a pilot study measuring electric fields. Measurements were made in the homes of 473 children who were diagnosed with a malignant neoplasm between 1992 and 1996 and who were aged 0-14 at diagnosis, together with 453 controls matched on age, sex and geographical location. Exposure assessments comprised resultant spot measurements in the child's bedroom and the family living-room. Temporal stability of bedroom fields was investigated through continuous logging of the 48-h vertical component at the child's bedside supported by repeat spot measurements. The principal exposure metric used was the mean of the pillow and bed centre measurements. For the 273 cases and 276 controls with fully validated measures, comparing those with a measured electric field exposure >/=20 V m(-1) to those in a reference category of exposure <10 V m(-1), odds ratios of 1.31 (95% confidence interval 0.68-2.54) for acute lymphoblastic leukaemia, 1.32 (95% confidence interval 0.73-2.39) for total leukaemia, 2.12 (95% confidence interval 0.78-5.78) for central nervous system cancers and 1.26 (95% confidence interval 0.77-2.07) for all malignancies were obtained. When considering the 426 cases and 419 controls with no invalid measures, the corresponding odds ratios were 0.86 (95% confidence interval 0.49-1.51) for acute lymphoblastic leukaemia, 0.93 (95% confidence interval 0.56-1.54) for total leukaemia, 1.43 (95% confidence interval 0.68-3.02) for central nervous system cancers and 0.90 (95% confidence interval 0.59-1.35) for all malignancies. With exposure modelled as a continuous variable, odds ratios for an increase in the principal metric of 10 V m(-1) were close to unity for all disease categories, never differing significantly from one. 相似文献
72.
Andrei V Alexandrov Martin Köhrmann Lauri Soinne Georgios Tsivgoulis Andrew D Barreto Andrew M Demchuk Vijay K Sharma Robert Mikulik Keith W Muir Gordon Brandt John Alleman James C Grotta Christopher R Levi Carlos A Molina Maher Saqqur Dimitris Mavridis Theodora Psaltopoulou Milan Vosko Peter D Schellinger 《Lancet neurology》2019,18(4):338-347
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Diet and nutrition are increasingly recognized as likely to be major determinants of cancer, notably cancers of the gastrointestinal tract, breast, endometrium, ovary, and prostate. Dietary factors may collectively account for a greater proportion of all cancers that occur in contemporary Western society than does any other category of environmental exposure (1). With the development of knowledge of the protective properties of certain components of food, links with diet have been suggested for other cancer sites (2). The epidemiological evidence for the association of diet and cancer is, however, not uniformly convincing; also, the likely biological pathways are not always clear. In this paper, we comment on some current hypotheses in this area and examine the best epidemiological methods to test them. 相似文献
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77.
Marsh JC; Will AJ; Hows JM; Sartori P; Darbyshire PJ; Williamson PJ; Oscier DG; Dexter TM; Testa NG 《Blood》1992,79(12):3138-3144
We have used the long-term bone marrow culture (LTBMC) system to analyze hematopoiesis in three patients with dyskeratosis congenita (DC), two of whom had aplastic anemia, and the third had a normal blood count (apart from mild macrocytosis) and normal BM cellularity. Hematopoiesis was severely defective in all three patients, as measured by a low incidence of colony-forming cells and a low level of hematopoiesis in LTBMC. The function of the marrow stroma was normal in its ability to support the growth of hematopoietic progenitors from normal marrows seeded onto them in all three cases, but the generation of hematopoietic progenitors from patients marrow cells inoculated onto normal stromas was reduced, thus suggesting the defect to be of stem cell origin. The parents and unaffected brother of one of the families have also been studied in LTBMC and all showed normal hematopoietic and stromal cell function. From this study we speculate that there are some similarities between DC and the defect in the W/Wv mouse. 相似文献
78.
To examine the relationship between early arrhythmias, infarctsize and prognosis, we compared 22 consecutive patients survivingacute myocardial infarction (AMI) and primary ventricular fibrillation(VF) with a control population after AMI uncomplicated by primaryVF. Left ventricular ejection fraction (EF) was measured byradionuclide ventriculography before discharge from hospital.Mean EF was significantly reduced below normal following AMIwith or without primary VF (normal 0.57±0.05, mean±SD;P<0.01). Mean EF was lower among patients who survived primaryVF than among those with infarction uncomplicated by primaryarrhythmia (0.33 ±0.12 v. 0.46 ±0.07; P<0.01).There were striking differences in EF between those patientswith anterior and those with inferior infarction. Mean EF forthose surviving primary VF after transmural anterior infarction(0.23±0.06) was lower than those who had primary VF aftertransmural inferior infarction (0.43±0.06; P<0.01J.Normal left ventricular function was seen in four individualswho developed no further complications. Recurrent primary ventriculararrhythmia was seen v only in those individuals subsequentlyshown to have reduced EF. Low EF (< 0-35) was seen in 12patients with primary VF in the context of anterior infarction,five developed breakthrough ventricular arrhythmias despitetherapy and in a limited follow-up period, three have died. 相似文献
79.
Saskia PJ Verkleij Pim AJ Luijsterburg Sten P Willemsen Bart W Koes Arthur M Bohnen Sita MA Bierma-Zeinstra 《The British journal of general practice》2015,65(637):e530-e537
Background
The effectiveness of diclofenac versus paracetamol in primary care patients with pain caused by knee osteoarthritis is unclear.Aim
To assess the effectiveness of diclofenac compared with paracetamol over a period of 2, 4, and 12 weeks in patients with knee osteoarthritis.Design and setting
Randomised controlled trial in general practice.Method
There were 104 patients included in the study, they were aged ≥45 years consulting their GP with knee pain caused by knee osteoarthritis. Patients were randomly allocated to diclofenac (n = 52) or paracetamol (n = 52) for at least 2 weeks. Primary outcomes were daily knee pain severity, and knee pain and function measured with the Knee Injury and Osteoarthritis Outcome Score (KOOS).Results
Over a period of 2- and 4-weeks follow-up, no significant difference in daily knee pain was found between the patient groups: estimated differences of 0.5 (95% CI = −0.2 to 1.3) and −0.2 (95% CI = −1.0 to 0.7), respectively. Over the 12-weeks follow-up, no significant differences were found between both groups for KOOS pain: estimated difference of −2.8 (95% CI = −10.7 to 5.1) and KOOS function of −2.7 (−10.6 to 5.0).Conclusion
Over a period of 2- and 4-weeks follow-up no significant difference in daily measured knee pain severity was found between primary care patients with knee osteoarthritis taking paracetamol or diclofenac. Also, over a period of 12-weeks follow-up no significant differences were found regarding KOOS pain and KOOS function between both groups. Patients more frequently reported minor adverse events after taking diclofenac (64%) than paracetamol (46%). 相似文献80.
Styles LA; Schalkwijk CG; Aarsman AJ; Vichinsky EP; Lubin BH; Kuypers FA 《Blood》1996,87(6):2573-2578
Acute chest syndrome (ACS) is associated with significant morbidity and is the leading cause of death in patients with sickle cell disease (SCD). Recent reports suggest that bone marrow fat embolism can be detected in many cases of severe ACS. Secretory phospholipase A2 (sPLA2) is an important inflammatory mediator and liberates free fatty acids, which are felt to be responsible for the acute lung injury of the fat embolism syndrome. We measured SPLA2 levels in 35 SCD patients during 20 admissions for ACS, 10 admissions for vaso-occlusive crisis, and during 12 clinic visits when patients were at the steady state. Eleven non-SCD patients with pneumonia were also evaluated. To determine if there was a relationship between sPLA2 and the severity of ACS we correlated SPLA2 levels with the clinical course of the patient. In comparison with normal controls (mean = 3.1 +/- 1.1 ng/mL), the non- SCD patients with pneumonia (mean = 68.6 +/- 82.9 ng/mL) and all three SCD patient groups had an elevation of SPLA2 (steady state mean = 10.0 +/- 8.4 ng/mL; vaso-occlusive crisis mean = 23.7 +/- 40.5 ng/mL; ACS mean = 336 +/- 209 ng/mL). In patients with ACS sPLA2 levels were 100- fold greater than normal control values, 35 times greater than values in SCD patients at baseline, and five times greater than non-SCD patients with pneumonia. The degree of SPLA2 elevation in ACS correlated with three different measures of clinical severity and, in patients followed sequentially, the rise in SPLA2 coincided with the onset of ACS. The dramatic elevation of SPLA2 in patients with ACS but not in patients with vaso-occlusive crisis or non-SCD patients with pneumonia and the correlation between levels of SPLA2 and clinical severity suggest a role for SPLA2 in the diagnosis and, perhaps, in the pathophysiology of patients with ACS. 相似文献