Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018799 (heart disease)
 34,133 document(s) hit in 31,850,051 MEDLINE articles (0.02 seconds)

Both cholesterol and polyunsaturated fatty acid (PUFA) metabolism play an important role in retinal and brain development and function. Dietary intake of cholesterol is accompanied with higher risk of heart disease and was suggested to have a role in the pathogenesis of Alzheimer's disease, while dietary PUFAs were reported to act in an opposite way. The same phenomena could be seen in case of inflammation. These effects are mainly realized through gene expression changes. In the present study, the effects of dietary cholesterol and the combination of cholesterol and fish oil were analyzed on the modulation of fatty acid composition and gene expression in the brain and in the eye. At the transcription level, specific changes could be detected in both tissues among transcription factor genes coding for sterol regulatory element binding proteins, retinoid X receptors and peroxisome proliferator-activated receptors, and different fatty acid binding protein genes by using quantitative real-time PCR. In the eye, cholesterol diet attenuated the positive effects of fish oil on inflammatory gene expression as the combined diet resulted in increased RNAm level of phospholipase A-2, inducible nitric oxide synthase, TNF-alpha, COX-1, COX-2 and cytokine, ICAM-1. This induction was absent in the brain. Complex changes could be also recorded in the fatty acid composition of lipids extracted from eye and brain tissue due to the dietary intervention. One of the most interesting changes was the reduced level of docosahexaenoic acid by cholesterol in the eye. Our results on fatty acid composition and gene expression changes may open up new alleys in understanding the complex roles of cholesterol and PUFAs in normal and pathological visual and brain function.
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PMID:Cholesterol and cholesterol plus DHA diet-induced gene expression and fatty acid changes in mouse eye and brain. 1558 91

In the last two decades, there has been a growing interest in unraveling the role that the Na+/Ca2+ exchanger (NCX) plays in the function and regulation of several cellular activities. Molecular biology, electrophysiology, genetically modified mice, and molecular pharmacology have helped to delve deeper and more successfully into the physiological and pathophysiological role of this exchanger. In fact, this nine-transmembrane protein, widely distributed in the brain and in the heart, works in a bidirectional way. Specifically, when it operates in the forward mode of operation, it couples the extrusion of one Ca2+ ion with the influx of three Na+ ions. In contrast, when it operates in the reverse mode of operation, while three Na+ ions are extruded, one Ca2+ enters into the cells. Different isoforms of NCX, named NCX1, NCX2, and NCX3, have been described in the brain, whereas only one, NCX1, has been found in the heart. The hypothesis that NCX can play a relevant role in several pathophysiological conditions, including hypoxia-anoxia, white matter degeneration after spinal cord injury, brain trauma and optical nerve injury, neuronal apoptosis, brain aging, and Alzheimer's disease, stems from the observation that NCX, in parallel with selective ion channels and ATP-dependent pumps, is efficient at maintaining intracellular Ca2+ and Na+ homeostasis. In conclusion, although studies concerning the involvement of NCX in the pathological mechanisms underlying brain injury during neurodegenerative diseases started later than those related to heart disease, the availability of pharmacological agents able to selectively modulate each NCX subtype activity and antiporter mode of operation will provide a better understanding of its pathophysiological role and, consequently, more promising approaches to treat these neurological disorders.
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PMID:Pharmacology of brain Na+/Ca2+ exchanger: from molecular biology to therapeutic perspectives. 1560 12

There are no new data in the Women's Health Initiative. The Collaborative Study of Hormone Factors in breast cancer showed a non-significant increased risk after 5 years. HERS showed an increased risk of cardiovascular disease in HT users with previous heart disease. The Cache County study indicated that estrogen therapy initiated after age 60 increased the incidence of Alzheimer's disease. The daily progestogen in the HT users decreased the estrogen receptors in the coronary arteries and minimized the beneficial direct effect of estrogen. It also decreased progesterone receptors in the endometrium, thus making it less endometrial-protective. The WHI was contrary to previous studies of estrogen therapy because women with specific menopausal symptoms were excluded, were older, had never used estrogen and had long-term estrogen deficiency. It takes healthy tissue to allow an effective response to estrogen and maintenance of health. Maximal benefit of HT may require early onset of treatment, near the time of menopause. However, it is never too late to arrest the progression of osteoporosis and decrease the risk of fracture.
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PMID:The women's health initiative reports in perspective: facts or fallacies? 1566 45

We present the results of the first theoretical investigation of salen-manganese complexes as synthetic catalytic scavengers of hydrogen peroxide molecules that mimic catalase enzymes. Catalase mimics can be used as therapeutic agents against oxidative stress in treatment of many diseases, including Alzheimer's disease, stroke, heart disease, aging, and cancer. A ping-pong mechanism approach has been considered to describe the H2O2 dismutation reaction. The real compounds reacting with a peroxide molecule were utilized in our BP density functional calculations to avoid uncertainties connected with using incomplete models. Part I of the dismutation reaction-converting a peroxide molecule into a water molecule with simultaneous oxidation of the metal atom of the catalyst-can be done quite effectively at the Mn catalytic center. To act as catalytic scavengers of hydrogen peroxide, the oxomanganese salen complexes have to be deoxidized during part II of the dismutation reaction. It has been shown that there are two possible reaction routes for the second part of the dismutation reaction: the top and the side substrate approach routes. Our results suggest that the catalyst could be at least temporarily deactivated (poisoned) in the side approach reaction route due to the formation of a kinetically stable intermediate. Overall, the side approach reaction route for the catalyst recovery is the bottleneck for the whole dismutation process. On the basis of the detailed knowledge of the mode of action of the (salen)MnIII catalase mimics, we suggest and rationalize structural changes of the catalyst that should lead to better therapeutic properties. The available experimental data support our conclusions. Our findings on the reaction dismutation mechanism could be the starting point for further improvement of salen-manganese complexes as synthetic catalytic scavengers of reactive oxygen species.
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PMID:(salen)MnIII compounds as nonpeptidyl mimics of catalase. Mechanism-based tuning of catalase activity: a theoretical study. 1573 83

Autism is a neurodevelopmental disorder that according to the Centers for Disease Control and Prevention (CDC) affects 1 in 150 children in the United States. Autism is characterized by impairments in social relatedness and communication, repetitive behaviors, abnormal movements, and sensory dysfunction. Recently emerging evidence suggests that mercury, especially from childhood vaccines, appears to be a factor in the development of the autistic disorders, and that autistic children have higher than normal body-burdens of mercury. In considering mercury toxicity, it has previously been shown that testosterone significantly potentates mercury toxicity, whereas estrogen is protective. Examination of autistic children has shown that the severity of autistic disorders correlates with the amount of testosterone present in the amniotic fluid, and an examination of a case-series of autistic children has shown that some have plasma testosterone levels that were significantly elevated in comparison neurotypical control children. A review of some of the current biomedical therapies for autistics, such as glutathione and cysteine, chelation, secretin, and growth hormone, suggests that they may in fact lower testosterone levels. We put forward the medical hypothesis that autistic disorders, in fact, represents a form of testosterone mercury toxicity, and based upon this observation, one can design novel treatments for autistics directed towards higher testosterone levels in autistic children. We suggest a series of experiments that need to be conducted in order to evaluate the exact mechanisms for mercury-testosterone toxicity, and various types of clinical manipulations that may be employed to control testosterone levels. It is hoped by devising therapies that address the steroid hormone pathways, in addition to the current treatments that successful lower heavy metal body-burdens of mercury, will work synergistically to improve clinical outcomes. In light of the fact that there are a number of other diseases that may have a chronic mercury toxicity component, such as Alzheimer's disease, heart disease, obesity, ALS, asthma, and other various forms of autoimmune disorders, it is imperative that further research should be conducted to understand mercury-testosterone toxicity.
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PMID:The potential importance of steroids in the treatment of autistic spectrum disorders and other disorders involving mercury toxicity. 1578 Apr 90

Dementia, a diagnostic syndrome that includes Alzheimer's disease (AD) and vascular dementia, affects more than 4 million Europeans. Its prevalence will increase as the population ages, even though half of cases remain undiagnosed. Dementia has a marked impact on the general health economy. The direct costs of caring for persons with AD alone exceed the cost of heart disease, cancer and stroke combined, primarily because of the need for expensive care in the later stages of the disease. Yet research spending for AD remains disproportionately small. Effective planning for the public health issues posed by AD mandates reduction of either the dependency or the prevalence of the disease. Some drug treatments have alleviated the symptoms of AD and improved the quality of life for patients and their families. However, many countries have introduced inappropriately stringent regulations for the use of medical therapy. These and related issues were addressed during the recent Facing Dementia Forum, in which 175 experts in dementia care discussed results of an extensive international survey. The experts identified three main barriers to effective care: (i) dementia is not considered a health care priority; (ii) there is a mistaken belief that nothing can be done about dementia; and (iii) early dementia is difficult to recognise. These observations provided a basis for the Agenda for Change, a series of strategies to overcome these barriers. The specific findings of the survey, as well as the Agenda for Change, will be reviewed in subsequent articles in this supplement.
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PMID:Is there a double standard when it comes to dementia care? 1580 Nov 84

Pathologically, Binswanger's disease is subcortical periventricular leucoencephalopathy sparing the U fibers. Clinically it is characterised by executive dysfunction, gait problems, urinary incontinence, pseudobulbar palsy, mood disturbances and dementia. The pathomechanism of Binswanger's disease is unclear. It is hypothesized that it results from an ischemic-hypoxic injury of the periventricular white matter, which, in turn, can be caused by a sclerotic elongation of the medullary arteries, widening of the perivascular spaces or decreased brain perfusion due to hypotension or heart disease. The symptoms of Binswanger's disease frequently overlap with those of normal pressure hydrocephalus, vascular parkinsonism and Alzheimer's disease. A diagnostic criterion of Binswanger's disease is radiologically demonstrated leukoaraiosis, which, on the other hand, is not equivalent with Binswanger's disease. A good clinical response after lumbar puncture or shunt implantation might lead to confusion with normal pressure hydrocephalus, which further complicates the clinical diagnosis. It is likely that among the above mentioned disorders there are a number of transitional forms and overlaps, which might be explained by the common pathomechanism of disturbance in cerebrospinal fluid circulation.
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PMID:[Clinico-pathology and differential diagnosis of Binswanger's disease]. 1588 11

Alpha-tocopherol, one of the eight isoforms of vitamin E, is the most potent fat-soluble antioxidant known in nature. For years, it was thought that alpha-tocopherol only functioned as a scavenger of lipid peroxyl radicals, specifically, oxidized low-density lipoprotein (oxLDL), thereby serving as a chief antioxidant for the prevention of atherosclerosis. In recent years, the many roles of alpha-tocopherol have been uncovered, and include not only antioxidant functions, but also pro-oxidant, cell signaling and gene regulatory functions. Decades of clinical and preclinical studies have broadened our understanding of the antioxidant vitamin E and its utility in a number of chronic, oxidative stress-induced pathologies. The results of these studies have shown promising, albeit mixed reviews on the efficacy of alpha-tocopherol in the prevention and treatment of heart disease, cancer and Alzheimer's disease. Future studies to uncover cellular and systemic mechanisms may help guide appropriate clinical treatment strategies using vitamin E across a diverse population of aging individuals.
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PMID:Alpha-tocopherol: roles in prevention and therapy of human disease. 1608 Dec 38

Alzheimer's disease is the third biggest killer in the developed world after cancer and heart disease. Although the first description dates back to almost a century ago, we still do not understand the cellular-molecular mechanisms that lead to the development of the brain pathology. There is no efficient treatment for the patients. And even the symptomatic relief comes too late, because there is no diagnostic method that could identify patients before severe clinical symptoms develop. Almost every aspect of Alzheimer's research, whether on pathogenesis, diagnosis, risk factors or treatment strategies, seem to spark controversy nowadays. Studies that apparently contradict one another or propose alternate explanations are published monthly. Patients' hopes are raised with the announcement of each new drug trial. Then hope is lost when the trials fail. Ironically, while progressive research is hampered by apparent contradictions and lack of funding, the old dogmas survive in the textbooks and no real progress is made in terms of therapy. The purpose of this review is to take stock of the most discussed and most strongly opposing views on the pathogenesis of Alzheimer's disease. These views shape the Alzheimer field currently and some will hopefully one day shape the diagnostic and therapeutic approaches to the disease.
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PMID:The last neuronal division: a unifying hypothesis for the pathogenesis of Alzheimer's disease. 1620 1

Even though the field of medicine has developed tremendously, the wide variety of cancer is still among chronic and life threatening disease today. Therefore, the specialists constantly research and try every possible way to find cure or preventive ways to stop its further development. For this reason, studies concerning the chronic disease such as cancer have been spread to many different fields. In this regard, many other alternative ways besides medicine, are used in prevention of cancer. Nutritional therapy, herbal therapy, sportive activities, art therapy, music therapy, dance therapy, imagery, yoga and acupuncture can be given as examples. Among these, dance/movement therapy which deals with individuals physical, emotional, cognitive as well as social integration is widely used as a popular form of physical activity. The physical benefits of dance therapy as exercise are well documented. Studies have shown that physical activity is known to increase special neurotransmitter substances in the brain (endorphins), which create a state of well-being. And total body movement such as dance enhances the functions of other body systems, such as circulatory, respiratory, skeletal, and muscular systems. Regarding its unique connection to the field of medicine, many researches have been undertaken on the effects of dance/movement therapy in special settings with physical problems such as amputations, traumatic brain injury, and stroke, chronic illnesses such as anorexia, bulimia, cancer, Alzheimer's disease, cystic fibrosis, heart disease, diabetes, asthma, AIDS, and arthritis. Today dance/movement therapy is a well recognized form of complementary therapy used in hospitals as well as at the comprehensive clinical cancer centres.
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PMID:Dance as a therapy for cancer prevention. 1623 9


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