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排序方式: 共有1339条查询结果,搜索用时 15 毫秒
51.
Lilia Bliznashka Joanne E. Arsenault Elodie Becquey Marie T. Ruel Deanna K. Olney 《Maternal & child nutrition》2020,16(1)
Anaemia is a persistent problem among young Burkinabe children, yet population‐specific information on its determinants is scant. We used baseline data from an evaluation of Helen Keller International's Enhanced Homestead Food Production Program (n=1210 children) to quantify household‐, mother‐, and child‐level factors associated with anaemia in Burkinabe children aged 6‐12 months. We used structural equation modelling to assess a theoretical model, which tested four categories of factors: (a) household food security and dietary diversity, (b) household sanitation and hygiene (latrine and poultry access and bednet ownership), (c) maternal factors (anaemia, stress, cleanliness, and health, hygiene and feeding knowledge and practices), and (d) child nutrition and health (iron deficiency (ID), retinol binding protein (RBP), malaria, and inflammation). The model also included household socio‐economic status, size, and polygamy; maternal age and education; and child age and sex. Results showed that ID, malaria, and inflammation were the primary direct determinants of anaemia, contributing 15%, 10%, and 10%, respectively. Maternal knowledge directly explained improved child feeding practices and household bednet ownership. Household dietary diversity directly explained 18% of child feeding practices. Additionally, RBP, child age and sex, and maternal anaemia directly predicted child haemoglobin. Our findings suggest that program effectiveness could be increased by addressing the multiple, context‐specific contributors of child anaemia. For young Burkinabe children, anaemia control programs that include interventions to reduce ID, malaria, and inflammation should be tested. Other potential intervention entry points suggested by our model include improving maternal knowledge of optimal health, hygiene, and nutrition practices and household dietary diversity. 相似文献
52.
Elodie Peyroux Marie-Nolle Babinet Costanza Cannarsa Charline Madelaine Emilie Favre Caroline Demily George A. Michael 《European child & adolescent psychiatry》2020,29(3):299-313
Impairments in social cognition have been frequently described in 22q11.2 deletion syndrome (22q11.2DS) and are thought to be a hallmark of difficulties in social interactions. The present study addresses aspects that are critical for everyday social cognitive functioning but have received little attention so far. Sixteen children with 22q11.2DS and 22 controls completed 1 task of facial expression recognition, 1 task of attribution of facial expressions to faceless characters involved in visually presented social interactions, and 1 task of attribution of facial expressions to characters involved in aurally presented dialogues. All three tasks have in common to involve processing of emotions. All participants also completed two tasks of attention and two tasks of visual spatial perception, and their parents completed some scales regarding behavioural problems of their children. Patients performed worse than controls in all three tasks of emotion processing, and even worse in the second and third tasks. However, they performed above chance level in all three tasks, and the results were independent of IQ, age and gender. The analysis of error patterns suggests that patients tend to coarsely categorize situations as either attractive or repulsive and also that they have difficulties in differentiating emotions that are associated with threats. An isolated association between the tasks of emotion and behaviour was found, showing that the more frequently patients with 22q11.2DS perceive happiness where there is not, the less they exhibit aggressive behaviour. 相似文献
53.
The immunosuppressive effect of CS-A was first studied in the assay for local GvHR. 3 x 106 viable spleen cells from LEW rats were injected into one foot pad of LEW x BN hybrids and both PLN were weighed 7 days later. Treatment of the recipients with 3 doses of 50 mg/kg/day of CS-A suppressed this local GvHR. The effect was more pronounced when treatment started at the time of cell transfer rather than a few days before peak response. In-vitro incubation of the cellular inoculum with CS-A also prevented local GvHR. Histology of the PLN confirmed the quantitative results expressed by the PLN index. CS-A was further investigated in the EAE model in LEW rats. It protected rats sensitised with spinal cord emulsified in complete Freund's adjuvant for as long as they were treated with CS-A. Treatment delayed until after the appearance of EAE also markedly improved their condition. Oral treatment of recipients with 50 mg/kg/day CS-A prevented the development of adoptive EAE following the transfer of lymphoid cells conditioned in vitro. The presence of 0.1-1.0 μg CS-A in the medium of the sensitised lymphoid cells also inhibited the adoptive transfer of EAE. Finally, if the cells for the adoptive transfer were derived from CS-A-treated sensitised donors, they failed to induce EAE. Histological examination supported the symptomatic findings 相似文献
54.
Moinard-Butot Fabien Poprawa Elodie Schohn Anna Pietro Addeo Benabdelghani Meher 《World Journal of Clinical Cases》2023,11(6):1372-1378
BACKGROUND Gemcitabine is an antimetabolite used in the treatment of pancreatic cancer. One of the side effects of gemcitabine is vascular toxicity. Here, we report the case of a patient treated with gemcitabine who had peripheral vascular disease concomitant with a prolonged antitumor response.CASE SUMMARY A 75-year-old man was diagnosed with locally recurrent pancreatic cancer. Partial response was achieved after 9 mo of gemcitabine. At the same time, the patient reported peripheral vascular d... 相似文献
55.
56.
Marc Le Vee Elodie Jouan Amélie Moreau Olivier Fardel 《Fundamental & clinical pharmacology》2011,25(1):99-103
Interferon (IFN)‐γ is known to downregulate expression of drug detoxifying proteins such as cytochromes P‐450 (CYPs) in human hepatocytes. The present study was designed to determine whether IFN‐γ may also impair expression of influx and efflux drug transporters, which constitute important determinants of the liver detoxification pathway. Exposure of primary human hepatocytes to 10 ng/mL IFN‐γ was found to downregulate mRNA levels of sinusoidal influx transporters such as sodium‐taurocholate cotransporting polypeptide, organic anion transporting polypeptide (OATP) 2B1, OATP1B1, and OATP1B3. IFN‐γ concomitantly reduced mRNA expression of drug efflux pumps such as multidrug resistance gene 1, multidrug resistance protein (MRP) 2, MRP3, breast cancer resistance protein and bile salt export pump. Such IFN‐γ‐mediated repression of major hepatic drug transporters may contribute to impaired liver clearance of drugs administrated to patients suffering from inflammation or viral infections associated with increased secretion of IFN‐γ. 相似文献
57.
58.
Gao XM Dilley RJ Samuel CS Percy E Fullerton MJ Dart AM Du XJ 《Journal of cardiovascular pharmacology》2002,40(4):632-640
This paper addresses whether the enhanced left ventricular (LV) contractility and heart rate, seen in transgenic mice overexpressing beta -adrenergic receptor in the heart, might raise the incidence of LV rupture after myocardial infarct. Transgenic and wild-type mice underwent left coronary artery occlusion. Postinfarct deaths that occurred 1-7 days after surgery were analyzed. Hemodynamics, morphologic parameters, and collagen content in the LV were determined. A significantly lower incidence of LV rupture was observed in transgenic than in wild-type mice 3-5 days after myocardial infarct (2.5 versus 19.7%, p < 0.05), despite a similar infarct size between the two groups and better hemodynamic function in transgenic mouse hearts. Morphologic analysis showed a more severe infarct expansion in wild-type versus transgenic mice or in mice dying of rupture versus those that died of acute heart failure. Collagen content was higher in the LV of sham-operated transgenic than wild-type mice (p < 0.01) with both type I and type III collagen elevated. Such difference in collagen content between transgenic and wild-type mice was maintained in noninfarcted and infarcted LV. In conclusion, transgenic mice overexpressing beta -adrenergic receptor had a lower risk of cardiac rupture during the acute phase after infarction despite the markedly enhanced LV contractility and heart rate. As a hyperdynamic function due to beta-adrenergic activation would likely increase the risk of cardiac rupture and infarct expansion, the lack of rupture in this transgenic mouse model suggests that the interstitial collagen level is a more important factor than functional status in the pathogenesis of rupture and infarct expansion. 相似文献
59.
Renal ischemia-reperfusion injury in the rat is prevented by a novel immune modulation therapy 总被引:3,自引:0,他引:3
Tremblay J Chen H Peng J Kunes J Vu MD Der Sarkissian S deBlois D Bolton AE Gaboury L Marshansky V Gouadon E Hamet P 《Transplantation》2002,74(10):1425-1433
BACKGROUND: Vasogen Inc.'s (Mississauga, Ontario, Canada) immune modulation therapy (IMT) is a therapy in which cells from the patient's own blood are modified by ex vivo exposure to specific physicochemical stressors, including oxidation, ultraviolet (UV) light, and an elevated temperature. The therapy has been shown to have a beneficial effect in models of inflammation and vascular diseases. This study tested the hypothesis that IMT can prevent renal ischemia-reperfusion (I/R) injury in rats. METHODS: Whole blood was collected from syngeneic age-matched donors by cardiac puncture. It was treated with a combination of controlled physiochemical stressors consisting of elevated temperature, a gas mixture of medical oxygen containing ozone, and UV light. The treated blood (150 microL) was injected in the gluteal muscle. Control animals received the same volume of untreated blood or physiological saline. Transient (45 or 60 minutes) left-renal ischemia was produced with simultaneous contralateral nephrectomy in treated and control spontaneously hypertensive rats (SHR). Young and old male and female rats were studied. Plasma creatinine, diuresis, and the survival rates of each group were compared. Renal apoptosis-necrosis was estimated by DNA laddering, histology, and in situ terminal deoxynucleotidyl transferase assay. mRNA levels of several regulators of apoptosis-regeneration were determined in control and postischemic kidneys by Northern blotting. RESULTS: IMT pretreatment of SHR significantly reduced renal I/R injury compared with equivalent placebo treatments consisting of untreated blood- or saline-injected SHR, as evidenced by a significant increase of the survival rate curves in young and old male SHR, which correlated with 24-hour postischemic diuresis. The increases in plasma creatinine following renal I/R were significantly lower in IMT-treated young male and old female SHR compared with saline or untreated blood-injected controls. Dilution analysis showed that the protective effect of treated blood was lost by dilution. Loss of epithelial cells was reduced in IMT-treated rats, with a significant decline in the peak of apoptosis 12 hours after acute ischemic renal injury. IMT did not modify the pattern of mRNA levels of several genes involved in the inflammation and regeneration processes. CONCLUSION: Our data demonstrate that IMT prevents the destruction of kidney tissue and the resulting animal death caused by renal I/R injury. 相似文献
60.