Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The nonviral gene delivery systems are usually not very effective in transferring gene into target cells, and the intensity and duration of the gene expression is very poor. The EBNA1/oriP maintain EBNA1/oriP-based plasmids as episome, contribute to nuclear transport of the plasmid and transcriptional up-regulation of target gene. The EBNA1/oriP based plasmid enhances the transfection rate as well as magnitude and longevity of gene expression. This article reviews recent preclinical gene therapy studies with the EBV plasmid vectors conducted against various diseases. For gene therapy against malignancies, the EBNA1/ oriP based plasmid encoding the HSV1-TK suicide gene was combined with a cationic polymer to transfer into HCC cell line. The expression level of TK gene was 100- to 1000-fold higher than the conventional plasmid. The sensitivity of HCC to ganciclovir (GCV) elevated several hundred-fold. The EBNA1/oriP based plasmid equipped with tumor specific promoter, such as CEA promoter, enabled targeted killing of CEA-positive tumor cell. Transfection of EBNA1/oriP based plasmid carrying IL-12 and IL-18 gene either locally, or systemically, induced therapeufic antitumor immune responses including augmentation of the cytotoxic T lymphocyte and natural killer activities and growth retardation of tumors. For gene therapy of congenital diseases and chronic diseases, the EBNA1/oriP based plasmid encoding the adenosine deaminase gene was transfered into human hematopoietic progenitor cells. The ADA activity was elevated 1.5-to 2-fold. Intracardiomuscrlar transfer of the EBNA1/oriP based plasmid encoding the beta-AR gene may be useful for the treatment of severe heart failure. Human tumor necrosis factoralpha (hTNFalpha) is one of the most important inflammatory cytokines. It has been implicated in many autoimmune and inflammatory diseases. sTNFR can efficiently neutralize the bioactivities of hTNFalpha. In primary study we cloned the chimeric protein sTNFR II-IgG Fc and expect to use it in the gene therapy of the inflammatory disease relative to TNF. In summary, The EBNA1/oriP based plasmid shows advantage in gene therapy of cancer, congenital and inflammatory diseases. Moreover, the EBNA1/oriP element may greatly contribute to the engineering of a human artificial chromosome, the ultimate device for controllable gene therapy.
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PMID:[Progress of EBNA1/oriP-based plasmid applied in gene therapy]. 1610 85

Chronic fatigue syndrome (CFS) is a debilitating illness affecting thousands of individuals. At the present time, there are few studies that have investigated causes of death for those with this syndrome. The authors analyzed a memorial list tabulated by the National CFIDS Foundation of 166 deceased individuals who had had CFS. There were approximately three times more women than men on the list. The three most prevalent causes of death were heart failure, suicide, and cancer, which accounted for 59.6% of all deaths. The mean age of those who died from cancer and suicide was 47.8 and 39.3 years, respectively, which is considerably younger than those who died from cancer and suicide in the general population. The implications of these findings are discussed.
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PMID:Causes of death among patients with chronic fatigue syndrome. 1684 74

It is a common practice to perform percutaneous or open coronary artery revascularisation in CHD to prevent sudden or unexpected death. Such a practice assumes that sudden and unexpected death is common in stable patients with uncomplicated CHD. This is a retrospective analysis of 248 patients (199, 80% men, 49, 20% women) who had median age 65.1 when assessed after stabilisation of their CHD and were followed up to 25 years until their death. Myocardial revascularisation was only performed after the patients had stabilised if they developed either progressive clinical disability or acute coronary syndromes. At stabilisation, 181 (73%) were uncomplicated, 59 (24%) had heart failure (HF) and 8 (3%) had other comorbidities. At their last visit before death, 67 (27%) were uncomplicated, 121 (49%) had HF, 41 (17%) had cancer and 19 (8%) had other comorbidities. Their median age at death was 72.4 years. 77 (31%) died suddenly, 47 (19%) of HF, 39 (16%) of cancer, 35 (14%) of acute myocardial infarction (AMI) and 50 (20%) had miscellaneous modes of dying. Unexpected death occurred in 26 (10%) of cases: sudden 12, AMI 7, stroke 3, suicide 2, abdominal aneurysm 1, motor vehicle accident 1. We conclude that the clinical condition of most patients with CHD deteriorates between their initial stabilisation and their final visit before their death-metamorphosis. Only a small proportion of deaths occur in patients with stable CHD and no HF. Intervention in stable patients without CHF is unlikely to reduce sudden or unexpected death in patients with CHD.
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PMID:Metamorphosis: the natural history of coronary heart disease. Sudden death is common. Unexpected death is not. 1690 70

We experienced and report a case where the patient was clinically diagnosed as depressive state which developed after being stung by a lumpfish-a kind of Japanese stonefish (Inimicus japonicus). Stonefish venom causes various symptoms ranging from local swelling with pain to general disturbances such as respiratory and heart failure with marked hypotension, cardiac perturbation, and neurologic damage including general seizure and coma. In the current case, the patient complained of local swelling with pain in the early stage, but subsequently he developed depressive state, and finally he began to have suicidal idea. When a patient is encountered who expresses severe depressive symptoms with suicidal idea, we hope that the patient can be examined by a psychiatrist, since the patient may have a serious accident or commit suicide during the process of the disease. On the other hand, it is easy to miss such depressive patients in cases where the depressive state appears after the appearance of toxic symptoms, and this is especially true in cases where the patient seems to be recovering naturally. In conclusion, we hope that medical institutions cooperate in analyzing the pathology of this toxicosis, since each institution rarely encounters such depressive patients.
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PMID:[Case clinically diagnosed as depressive state after being stung by a lumpfish (Inimicus japonicus)]. 1713 82

There are many causes of sudden death ranging from accidents and suicide to vascular events and arrhythmias. Most sudden deaths will occur in people who have not been diagnosed with a serious heart condition but at a very low annual rate. Many of these events are probably vascular and might be prevented by reducing the risk of developing coronary disease. Only a minority of sudden deaths occur in people with established cardiac disease, but in patients with major structural heart disease, the annual rate is high. The causes of sudden death are many in this clinical setting also, but dominated by ventricular arrhythmias and vascular events. There is good evidence that conventional treatments for heart failure, including ACE inhibitors, beta-blockers, aldosterone antagonists and cardiac resynchronization devices reduce the risk of sudden death. Evidence that statins, aspirin or revascularisation are safe or effective in patients with heart failure is currently lacking. Implantable defibrillators confer a small but definite additional survival advantage by treating arrhythmias that have not been prevented.
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PMID:Fighting against sudden death: a single or multidisciplinary approach. 1741 28

Clinical heart failure results from the cumulative loss of functioning myocardium from any cause. At the cellular level, cardiac myocytes die from three causes, individually or in combination: Necrosis occurs when external conditions are not sufficient to sustain minimal cellular functions, as with ischemia, and there is a general and unorganized breakdown of cell organelles, engendering an inflammatory response that may have harmful collateral tissue effects. Apoptosis, or cell suicide, occurs when specific external or internal conditions provoke a highly structured sequence of events to shut down cellular functions and remove the cell, with minimal consequences to surrounding tissue. Autophagy is a normal response to cell starvation that is induced under conditions of chronic metabolic or other stress. Current therapeutics, such as early myocardial revascularization after myocardial infarction, are focused exclusively upon minimizing cardiac myocyte necrosis and may even contribute to secondary apoptosis and autophagy. This review explores possible approaches to bring cardiac myocytes that are destined to die, back to life, i.e., cellular resuscitation. Two pro-apoptotic proteins in particular, Bnip3 and Nix, are transcriptionally upregulated specifically in response to myocardial ischemia and pathological hypertrophy and have been examined as therapeutic targets. In Bnip3 and Nix genetic mouse models, prevention of cardiac myocyte apoptosis in ischemic and hemodynamically overloaded hearts salvaged myocardium, minimized late ventricular remodeling, and enhanced ventricular performance. Cardiomyocyte resuscitation by preventing programmed cell death shows promise as an additive approach to minimizing necrosis for long-term prevention of heart failure.
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PMID:The rationale for cardiomyocyte resuscitation in myocardial salvage. 1856 79

Autophagy is a cell survival mechanism that involves degradation and recycling of cytoplasmic components, such as long-lived proteins and organelles. In addition, autophagy mediates cell death under specific circumstances. Apoptosis, a form of programmed cell death, has been well characterized, and the molecular events involved in apoptotic death are well understood. Damaged cardiomyocytes that show characteristics of autophagy have been observed during heart failure. However, it remains unclear whether autophagy is a sign of failed cardiomyocyte repair or is a suicide pathway for the failing cardiomyocytes. Although autophagy and apoptosis are markedly different processes, several pathways regulate both autophagic and apoptotic machinery and autophagy can cooperate with apoptosis. This review summarizes the evidence for crosstalk between autophagy and apoptosis.
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PMID:Crosstalk between autophagy and apoptosis in heart disease. 1870 86

Apoptosis is a biological process of death or cellular suicide present in all the cells of the metazoans. It maintains the balance between the regeneration of pluripotential cells -or stem cells- and the elimination of cells that have already served their function, of cells that have reproduced in excess, or have been genetically damaged beyond repair. Apoptosis activation in cardiomyocytes is a common problem in a large variety of cardiomyopathies; it has been suggested that it is an important contributor ventricular hypertrophy and to the increase of the infarct size in patients with cardiac failure and cardiovascular disease. Clinical diagnosis of apoptosis is a reality in the medical science, its application in different aspects of cardiology includes from coronary cardiopathy to rhythm alterations. In this sense, the use of the non-invasive imaging, can be very useful for the in vivo detection of this type of cellular death in patients with myocardial necrosis, acute myocardial infarct, acute rejection of cardiac transplantation, myocarditis, intracardial malignant tumours, as well as in cardiotoxicity cases and other cardiomyopathies. Particularly, binding of Tc99m-labeled Annexin V, produces gammagraphic images that allow the identification of apoptotic cells in vivo in SPECT and SestaMiBi systems. In summary, the use of these techniques will be invaluable in the near future for anti-apoptosis therapy and intervention in the routine of the daily Cardiology practice.
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PMID:[Apoptosis detection in cardiovascular diseases through nuclear cardiology SPECT images]. 1875 13

Autophagy has evolved as a conserving process that uses bulk degradation and recycling of cytoplasmic components, such as long-lived proteins and organelles. In the heart, autophagy is important for the turnover of organelles at low basal levels under normal conditions and it is upregulated in response to stresses such as ischemia/reperfusion and in cardiovascular diseases such as heart failure. Cardiac remodeling involves increased rates of cardiomyocyte cell death and precedes heart failure. The simultaneously occurring multiple features of failing hearts include not only apoptosis and necrosis but also autophagy as well. However, it has been unclear as to whether autophagy is a sign of failed cardiomyocyte repair or is a suicide pathway for failing cardiomyocytes. The functional role of autophagy during ischemia/reperfusion in the heart is complex. It has also been unclear whether autophagy is protective or detrimental in response to ischemia/reperfusion in the heart. In this review, we will summarize the role of autophagy in the heart under both normal conditions and in response to stress.
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PMID:The role of autophagy in the heart. 1900 22

The molecular and cellular basis for cardiac remodeling have been difficult to establish. Transcriptional analysis and genetic manipulation of the mouse heart have revealed expression of a molecular program for cardiac myocyte suicide under conditions of myocardial injury or hemodynamic stress. Interrupting the cardiomyocyte suicide program by selective ablation of inducible apoptosis genes has proven to be remarkably effective in preventing remodeling and heart failure following myocardial infarction. Since these apoptotic genes are similarly dysregulated in human heart disease, the stage is set for a new era of therapeutics targeting cardiac suicide genes and their products.
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PMID:Having a change of heart: reversing the suicidal proclivities of cardiac myocytes. 1976 77


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