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51.
Heather M Arthur Christine Patterson James A Stone 《European journal of cardiovascular prevention and rehabilitation》2006,13(1):3-9
BACKGROUND: Presently, complementary and alternative medicine, including both therapies and herbal/oral supplements, is used globally. Few studies have examined the use of specific therapies, separate from herbal/oral supplements, in cardiac rehabilitation. This paper presents a systematic evaluation of current research evidence related to use of specific complementary and alternative medicine therapies in secondary prevention of cardiovascular disease, with a view to making recommendations for cardiac rehabilitation. DESIGN AND METHODS: A literature search was conducted using complementary and alternative medicine websites, Medline, Allied and Complementary Medicine, CINAHL, Cochrane databases, EMBASE, SportDiscus, Clinical Evidence, and Evidence-Based Practice to locate research-based scientific evidence related to the use of complementary and alternative medicine in cardiac rehabilitation. Search keywords included heart, cardiac, cardiovascular, coronary, myocardial and rehabilitation, combined with particular therapies. Herbal/oral supplements were not included in this evaluation. RESULTS: Some complementary and alternative medicine therapies may be useful to patients by themselves or coupled with traditional cardiac rehabilitation. Tai chi, as a complement to existing exercise interventions, can be utilized for low and intermediate risk patients. transcendental meditation may be used as a stress reduction technique. There was insufficient evidence found for the use of acupuncture or chelation therapy in cardiac rehabilitation or secondary prevention. CONCLUSIONS: Some complementary and alternative medicine therapies hold promise for patients in cardiac rehabilitation. Further research is essential, however, in all areas of complementary and alternative medicine to confirm its usefulness as an adjunct to cardiac rehabilitation. 相似文献
52.
53.
James R. Gill 《Forensic science, medicine, and pathology》2006,2(1):29-32
On September 11, 2001 two hijacked airplanes struck the Twin Towers at the World Trade Center in New York City. All of the
remains (19,915) were examined by the Office of Chief Medical Examiner (OCME) of New York City. The major goals of the OCME
were to accurately identify the decedents and to promptly issue death certificates. As of September 2005, there were 1594
identifications of a total of 2749 people reported missing. Of these, 976 were identified by a single means, which included
DNA analysis in 852 of the victims. Use of legal statues can assist in the timely issuance of death certificates in mass fatalities,
which benefit surviving family members. DNA analysis markedly improves the ability to identify remains and has become the
standard method for identification in these types of disasters. Certain postmortem tissue samples are better suited for DNA
analysis and yield better results than others. 相似文献
54.
Hepatic gene downregulation following acute and subchronic exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin. 总被引:1,自引:0,他引:1
Bladimir J Ovando Chad M Vezina Barbara P McGarrigle James R Olson 《Toxicological sciences》2006,94(2):428-438
Chronic exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) has been shown to lead to the development of hepatotoxicity and carcinogenicity in the liver of female rats. In this study, we investigated hepatic gene downregulation in response to acute and subchronic TCDD exposure. We identified 61 probes which exhibited a downregulation of twofold or greater following subchronic (13 weeks) exposure to TCDD. Comparative analysis of the hepatic expression of these 61 probes was conducted with rats subchronically exposed to PeCDF, PCB126, PCB153, and a mixture of PCB126 and PCB153. PCB153 produced little or no alteration in these probes, while the binary mixture mimicked most closely the downregulation observed with TCDD. To discern if the repression of genes within this probe set occur as a primary response to TCDD exposure, we analyzed the early responsiveness of 11 genes at 6, 24, and 72 h following a single exposure to TCDD. We observed early repression of the 11 genes within this early time course, indicating that the repression of this subset of genes occurs as a primary response to TCDD exposure and not as a secondary response to 13 weeks of subchronic treatment. In addition, the gender, species, and AhR dependence of these responses were also investigated. Gender- and species-dependent repression was observed within this subset of genes. Furthermore, utilizing AhR knockout mice, we were able to determine the AhR-dependent downregulation of seven of 11 genes. Together these results assist efforts to understand the multitude of effects imposed by TCDD and AhR ligands on gene expression. 相似文献
55.
To determine if impaired energy metabolism might contribute to some aspects of Alzheimer disease (AD), including the vulnerability of the CA1 region of the hippocampal formation and the altered cytoskeleton evident in neurofibrillary tangles, we examined the effects of metabolic poisons on neuronal damage and cytoskeletal disruption in the hippocampal formation. Intrahippocampal injection of 3-nitropropionic acid (3-NP) and malonic acid resulted in neuronal death, particularly in CA1. Cytoskeletal disruption included loss of dendritic MAP2, but sparing of axonal τ. MK-801 (a noncompetitive NMDA receptor antagonist) did not atenuate the lesions produced by intrahippocampal injection of malonate. MK-801, however, was effective against intrastriatal malonate. Acute systemic 3-NP resulted in neuronal damage and cytoskeletal disruption in the CA1 region of the hippocampal formation, including an extensive loss of MAP2 immuno-reactivity, but sparing of τ. The neuronal loss in CA1 was delayed as compared to striatum. Chronic intraventricular infusion of 3-NP produced a different pattern of neuronal damage. Loss of τ-1 immuno-reactivity was observed in CA3 and CA1 s. oriens, whereas MAP2 immunostaining was preserved. These results demonstrate that chronic and acute administration of metabolic inhibitors produce distinct patterns of neuronal damage and cytoskeletal disruption. The results further suggest a differential involvement of the NMDA receptor in malonate-induced neuronal damage in striatum as compared to the hippocampus. The pattern of neuronal damage and cytoskeletal disruption observed following acute metabolic impairment resembled some aspects of neurofibrillary pathology in AD, but did not result in τ hyperphosphorylation. 相似文献
56.
Calcified tissue is a common component of atherosclerotic plaques, and occurs most often in mature plaques. The process of calcification is a poorly understood risk factor that may contribute to a plaque's vulnerability to sudden rupture. In this study a solid-state imaging sequence, termed single-point imaging (SPI), was used to observe calcification directly in ex vivo atherosclerotic plaques. Standards were used to validate the ability of (31)P SPI to detect and differentiate calcification from crystalline cholesterol, phospholipids, and other plaque components. After suitable experimental parameters were found, human carotid specimens obtained by endarterectomy were imaged ex vivo by (31)P solid-state imaging and standard (1)H methods. In contrast to (1)H imaging methods, (31)P imaging detected only the calcification in the plaque. 相似文献
57.
Daoyan Wei Henry Q. Xiong James L. Abbruzzese Keping Xie 《Journal of gastrointestinal cancer》2003,33(1):43-60
Pancreatic cancer is a lethal disease characterized by early metastasis, local invasion, and resistance to conventional therapies. To understand its etiology and eventually make prevention of it possible and effective, appropriate carcinogenesis models will certainly help us understand the effects of environmental and genetic elements on pancreatic carcinogenesis. The development of new treatment strategies to control cancer metastasis is of immediate urgency. Fulfillment of this task relies on our knowledge of the cellular and molecular biology of pancreatic cancer metastasis and the availability of biologically and clinically relevant model systems. Many of the existing pancreatic cancer carcinogenesis and metastasis animal models are described in this review. The advantages and disadvantages of each model and their clinical implications are discussed, and special attention is focused on experimental therapeutic strategies targeting pancreatic cancer metastasis. 相似文献
58.
59.
Turboprop: improved PROPELLER imaging. 总被引:1,自引:0,他引:1
A variant of periodically rotated overlapping parallel lines with enhanced reconstruction (PROPELLER) MRI, called turboprop, is introduced. This method employs an oscillating readout gradient during each spin echo of the echo train to collect more lines of data per echo train, which reduces the minimum scan time, motion-related artifact, and specific absorption rate (SAR) while increasing sampling efficiency. It can be applied to conventional fast spin-echo (FSE) imaging; however, this article emphasizes its application in diffusion-weighted imaging (DWI). The method is described and compared with conventional PROPELLER imaging, and clinical images collected with this PROPELLER variant are shown. 相似文献
60.
Mary Ann Richardson Helen M Chao Laura L Read James D Clelland Raymond F Suckow 《American journal of medical genetics. Part B, Neuropsychiatric genetics》2006,(2):195-197
Phenylketonuria (PKU), an inborn error of phenylalanine metabolism, has been shown to be a risk factor for tardive dyskinesia (TD). In male psychiatric patients there was a significant relationship between TD and measures of plasma phenylalanine following ingestion of a standardized phenylalanine dose that was indicative of higher brain availability of phenylalanine in patients with TD. In addition, a medical food formulation consisting of branched chain amino acids, which compete with phenylalanine for transport across the blood-brain barrier, has been demonstrated to be an efficacious treatment for TD. Cumulatively these findings suggested that TD was related to phenylalanine metabolism and thus that sequence variants in the gene for phenylalanine hydroxylase (PAH), the rate-limiting enzyme in the catabolism of phenylalanine, could be associated with TD susceptibility. Genetic screening of PAH in a group of 123 psychiatric patients revealed ten sequence polymorphisms and two mutations, but none appeared to be a significant risk factor for TD. 相似文献