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Biomedical subjects

T Ogihara

Publications and source records attributed to T Ogihara.

At least 109 records · Page 6Linked to original sources
PubMed2001

[A case of severe systemic edema in an elderly hypertensive patient with systemic lupus erythematodes during long-term treatment with anti-hypertensive drugs].

A 71-year-old woman receiving both angiotensin II receptor antagonist and calcium antagonist suffered severe systemic edema. She had been treated for essential hypertension with amlodipine for 2 years and candesartan for 3 months, and systemic lupus erythematodes (SLE) with steroids. During treatment, severe systemic edema appeared, mainly on her face, arms, and legs. At first, we suspected drug-induced edema by candesartan, so it was halted, but the edema still continued. We then considered amlodipine to be the culprit, and finally, the severe systemic edema disappeared after cessation of amlodipine. To control her blood pressure, we recommended candesartan, but 3 months late she suffered severe systemic edema again, thus the causative we drugs of her edema were thought to be both amlodipine and candesartan. Edema is a common symptom in elderly patients and we frequently observe drug-induced edema. In this case, there was underlying acceleration of blood vessel permeability induced by SLE and steroids and moreover, vasodilatation by candesartan and/or amlodipine further accelerated blood vessel permeability, and thus might have caused severe edema. It is very difficult to determine the cause of edema, especially in elderly patients, but we should consider not only one but also two or more drugs as being involved in drug-induced edema.

Aged↗
PubMed2001

[Gene therapy for arteriosclerotic diseases].

Recent progress in molecular biology gives us gene therapy, as a new strategy for treatment of cardiovascular diseases. Targeted diseases have been wide-spread from single gene-deficient diseases to more complexed adult diseases such as restenosis after angioplasty and ischemic diseases. Clinical gene therapy for restenosis and angina using VEGF gene have already performed in USA and they can show beneficial effects of such strategies. On the other hand, we have just started a clinical trial using E2F decoy for restenosis after PTA or PTCA, since April 2000. E2F decoy is expected to become a new treatment for restenosis as a gene therapy. Also, the feasibility of a novel therapeutic strategy using angiogenic growth factors such as VEGF to augment collateral artery development has recently entered the realm of treatment of ischemic diseases. We focus on HGF, which is a novel endothelial growth factor. HGF-based therapeutic angiogenesis would possibly result a new treatment for severe ischemic diseases.

Angioplasty, Balloon, Coronary↗
PubMed2001

Symposium on the etiology of hypertension--summarizing studies in 20th century. 1. Hypertension and genes.

Under classical strategy, scientists have tried first to find a physiological phenomenon specific for essential hypertension, then to identify the protein underlying the physiological abnormality, and finally to clarify the causative gene which encoded the protein. On the other hand, under the reverse genetic approach, the correlation between hypertension and genetic abnormality is identified first, and then the pathogenesis is clarified-in reverse order. Therefore, it is not extraordinary for unexpected results to be obtained in the correlation between a gene and a disease, suggesting that this approach has a possibility to be a breakthrough in the chaos of hypertension research.

Angiotensinogen↗
PubMed2001

[Genetic polymorphisms of the renin-angiotensin system].

Essential hypertension is a multifactorial disease which is evoked by multiple environmental and genetic factors. Recent progress in molecular biology enables us a comprehensive understanding of the molecular pathogenesis of this disease. The genes of renin-angiotensin system such as renin, angiotensinogen, angiotensin-converting enzyme and angiotensin receptors genes are all reported as positive linkage to hypertension. Now ongoing progress of the human genome project will further accelerate the molecular studies on the rennin-angiotensin system and hypertension.

Angiotensinogen↗
PubMed2001

[Antihypertensive treatment guideline for elderly hypertension].

Recently published Hypertension Treatment Guideline by Japanese Society of Hypertension (JSH2000) contains several unique suggestions for treatment of elderly hypertension in particular. In general, the therapeutic goal of blood pressure in the elderly is set at a higher level than that in the young. For the patients of age 70 and over blood pressure should be controlled less than 150-160 mmHg. The following drugs are recommended as the first line drug in the elderly hypertension: 1. long-acting Ca antagonists, 2. ACE inhibitors (or angiotensin II antagonists) and 3. small dose of diuretics. Combination therapy should be considered when monotherapy of more than 2 to 3 months is not successful to reduce blood pressure below 150/90 mmHg.

Aged↗
PubMed2001

[Review of randomized trials of angiotensin receptor blockers in the treatment of patients with congestive heart failure].

Angiotensin-converting enzyme (ACE) inhibitors are the first-line drugs for the treatment of congestive heart failure, but many patients could not receive those benefits because of intolerance. Recent randomized trials of angiotensin receptor blockers (ARB) in the treatment of patients with congestive heart failure elucidated clinical benefits of ARB as well as ACE inhibitors. ELITE II showed equivalent effect on mortality and morbidity between losartan and captopril and less adverse events in losartan. Val-HeFT showed additive benefits of valsartan on standard treatment with ACE inhibitors, diuretics and digitalis in patients with heart failure. CHARM would be elucidate the clinical usefulness of candesartan cilexetil in a broad spectrum of patients with symptomatic heart failure including patients whose LVEF greater than 40%.

Angiotensin Receptor Antagonists↗
PubMed2001

Lack of association between hepatocyte nuclear factor-1beta gene and common forms of type 2 diabetes in the Japanese population.

Mutations in the hepatocyte nuclear factor-1beta (HNF-1beta) gene have been shown to be a cause of maturity-onset diabetes of the young (MODY). We studied the contribution of the HNF-1beta gene to susceptibility to common forms of Type 2 diabetes in the genetically homogeneous Japanese population, by investigating the allelic association of Type 2 diabetes with two markers in the HNF-1beta region. The frequency of a nonsense mutation, R177X, which was previously reported in a Japanese family, was also studied by the polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) method using a mismatch primer. A total of 200 subjects were studied. There was no significant difference in allele frequencies of either of the two polymorphisms studied between patients with Type 2 diabetes and control subjects, or between subgroups of patients subdivided by the presence of mild or severe diabetic nephropathy. None of the subjects studied had R177X mutation, giving a frequency of less than 1.1% in common forms of Type 2 diabetes in Japan. These results suggest that mutations in the HNF-1beta gene derived from a limited number of founders are not a major cause of common forms of Type 2 diabetes, even in the genetically homogeneous Japanese population.

Adult↗
PubMed2001

[HGF as a key molecule in cardiovascular diseases].

Hepatocyte growth factor(HGF) is focused as a powerful endothelial growth factor in the field of cardiovascular diseases. As its physiological role in atherosclerosis, restenosis, angiogenesis etc is very important, HGF-based new treatments for various diseases are expected. Clinical gene therapy for restenosis and ischemic diseases using VEGF gene have already performed in USA, and they could show beneficial effects of such strategies. In Japan, gene therapy using HGF gene for ASO has just begun in spring 2001. In near future, powerful therapeutic effects of HGF could applied to restenosis, graft failure, cardiomyopathy, cerebral vascular diseases, renal failure and so on.

Animals↗
PubMed2000

Activated cAMP-response element-binding protein regulates neuronal expression of presenilin-1.

Upon binding to the cAMP-response element of a gene's promoter, the transcription factor known as cAMP-response element-binding protein (CREB) facilitates transcription of many different neuronal genes including those involved with synaptic function. Based on our previous reports of gene structure (GenBank accession number AF029701 ), we now demonstrate that activated CREB binds to the proximal promoter of the human presenilin-1 (PS-1) gene to activate PS-1 transcription in rat and in human neuronal cells. Specific stimulation of the N-methyl-d-aspartate subtype of neuronal glutamate receptors activates CREB and results in increased PS-1 expression. Similarly, treatment with brain-derived neurotrophic factor activates CREB and increases PS-1 expression in a dose-dependent fashion. By using adenovirus vectors expressing dominant negative forms of CREB, we were able to show that induction of PS-1 expression requires the activation of CREB. Conversely, constitutive expression of mitogen-activated protein kinase/extracellular signal-regulated kinase (MEK) results in activation of CREB and increased PS-1 expression that can be blocked by the addition of selective MEK inhibitors. Our findings suggest a hypothesis where stimulation of N-methyl-d-aspartate receptors signals CREB activation to enhance PS-1 gene product expression that contributes to normal neuronal functions.

Adenoviridae↗