PubMed Health⌕ Search

Biomedical subjects

N Yoshimine

Publications and source records attributed to N Yoshimine.

At least 19 recordsLinked to original sources
PubMed1997

Clinical outcome of smoking-cessation trial of nicotine chewing gum evaluated by analysis of nicotine in hair.

The axial distribution of nicotine along the hair shafts was examined in 21 subjects enrolled in a placebo-controlled, double-blind trial of nicotine chewing gum (Nicorette) for validating their self-reported smoking behavior and their physicians' assessments. Hair samples obtained from the subjects once during the 3-month follow-up period (n = 10 for placebo and n = 11 for Nicorette ad libitum) were analyzed for the cm x cm distribution of nicotine along the hair shafts. Hair analysis results were compared with the monthly self-reports and with the plasma concentrations of thiocyanate (SCN-) measured at 1-month intervals. A gradual decrease in nicotine content along the hair shafts generally corresponded to the decrease in self-reported number of cigarettes smoked daily by the subjects who reported that they abstained from smoking or decreased the number of daily cigarettes in placebo and nicotine chewing gum groups. Because nicotine may dissociate slowly from hair follicle cells, nicotine in the hair did not mark a sudden decrease or cessation of smoking and, therefore, hair analysis tended to underestimate the real decrease of smoking. However, physician assessment seemed to depend solely on self-reporting because the time profile of changes in serum SCN- concentration did not correspond necessarily to the changes in the self-reported number of cigarettes used daily.

Adult↗
PubMed1994

Comparative toxicity of oxidatively modified low-density lipoprotein and lysophosphatidylcholine in cultured vascular endothelial cells.

Oxidative modification of low-density lipoprotein (LDL) may play an important role in the initiation and progression of atherosclerosis. We previously showed that the cytotoxicity of oxidized LDL (oxLDL) depended on the level of lipid hydroperoxides. Meanwhile, it has been shown that during LDL oxidation, a significant part of the LDL phosphatidylcholine (PC) is degraded to lysophosphatidylcholine (LPC) by an intrinsic phospholipase A2-like activity, and that LPC is toxic to various cells. In the present study, we compared the toxicity of oxLDL with that of LPC in cultured bovine aortic endothelial cells. Cytotoxicity induced by LPC, assessed by the release of lactate dehydrogenase (LDH), reached a plateau within 1 h. LDH release induced by oxLDL occurred much later, at about 3 h, and increased linearly until nearly all the LDH was released at 10 h. The addition of deferoxamine, a Fe3+ chelator, to the reaction medium prevented the toxic effects of oxLDL, but not of LPC. Native LDL and oxLDL inhibited the toxicity of LPC, while native LDL promoted the toxicity of oxLDL. Albumin inhibited the toxicity of LPC but not of oxLDL. Preincubation of endothelial cells with an antioxidant, probucol, protected against oxLDL toxicity, but not against LPC toxicity. These results suggest that lipid hydroperoxides associated with the oxLDL particle, not LPC, constitute the toxic moiety of oxLDL. These substances may generate lipid peroxyl and alkoxyl radicals in the presence of ionic iron, probably from intracellular iron stores in endothelial cells, and produce cytotoxicity.

Animals↗
PubMed1993

Dexamethasone-induced suppression of aortic atherosclerosis in cholesterol-fed rabbits. Possible mechanisms.

We investigated the mechanisms by which corticosteroids affect atherosclerosis. Male New Zealand White rabbits were injected with 0.125 mg dexamethasone (n = 10) or vehicle (control group, n = 10). Both groups were fed a 1% cholesterol diet for 8 weeks. Although the dexamethasone-treated animals exhibited a greater degree of hyperlipidemia, they exhibited significantly less atherosclerotic plaque of the aortic surface than control animals (7.8% versus 47.2%). Immunofluorescence study of the aortic plaque specimens showed that dexamethasone administration reduced both macrophages and T lymphocytes. In vitro, dexamethasone suppressed the proliferation and differentiation of U937 cells and inhibited uptake and degradation of beta-very low density lipoproteins by mouse peritoneal macrophages. These findings suggest that dexamethasone suppresses the development of atherosclerosis in the aorta of rabbits by inhibiting recruitment and proliferation of macrophages and the formation of foam cells in plaques.

Animals↗
PubMed1993

[A case of indomethacin-inhibited recurrent periodical attacks of Mollaret's meningitis].

A 65-year-old woman was admitted to our hospital on May 28, 1990, because of recurrent high fever, over 39 degrees C, headache and general fatigue. In June 1988, she suffered the first episode of high fever, headache and general fatigue. Since then, those symptoms attacked her recurrently at intervals of 7 to 10 days. She was admitted to a hospital for two months in 1988. However, the etiology was unclear and treatment, including antibiotics, was not effective. After admission to our hospital, the symptoms of high fever, headache and general fatigue developed suddenly, lasted for 2 to 4 days, then disappeared spontaneously. These symptoms recurred periodically at intervals of 7 to 10 days. Findings of lumbar puncture during the period with severe symptoms revealed a leukocytic pleocytosis (polymorphonuclear neutrophil count: 1,324/3 mm3, mononuclear cell count: 48/3 mm3, without Mollaret cells) increased protein (0.81 g/l) and decreased glucose (0.28 g/l). Cerebrospinal fluid (CSF) examination during the period without symptoms showed a dramatic decrease of pleocytosis (polymorphonuclear neutrophil count: 5/3 mm3, mononuclear cell count: 17/3 mm3, without Mollaret cells) with improved protein (0/64 g/l) and glucose (0.40 g/l). Various examinations revealed no evidence of infection, malignancy, collagen disease, endocrine disease or any disorders in the nervous system. Moreover, bacterial cultures of blood and CSF were negative and a brain CT scan showed no abnormal findings. We diagnosed this case as Mollaret's meningitis and gave 25 mg indomethacin after every meal (75 mg/day). Her symptoms were improved abruptly and the duration of symptoms shortened and symptom-free intervals became longer.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗
PubMed1993

Protective effects of idebenone on vascular endothelial cells against toxicity induced by oxidatively modified low density lipoprotein.

We examined the protective effects of idebenone, 6-(10-hydroxydecyl)-2,3-dimethoxy-5-methyl-1,4-benzoquinone, on the cytotoxicity of oxidatively-modified low density lipoprotein (oxLDL), using cultured vascular endothelial cells from fetal bovine aorta. When the cells were incubated with idebenone, the toxicity of oxLDL was inhibited dose-dependently (10(-7)-10(-5) M). When cells were preincubated with idebenone, the toxicity of oxLDL was inhibited only at a high concentration (10(-5) M). However, idebenone had no significant effects on copper-induced modification of LDL. The protective effects of idebenone on oxLDL-induced endothelial toxicity may be beneficial for the inhibition of the development of atherosclerosis in the brain and other arterial systems.

Animals↗
PubMed1993

Effects of dexamethasone on migration of human monocytes in response to oxidized beta-very low density lipoprotein.

OBJECTIVE: We previously showed that dexamethasone inhibited the development of atherosclerosis in cholesterol-fed rabbits. In the present study, we investigated the mechanisms of this inhibition. METHODS: Monocytes were isolated from the peripheral blood of healthy donors. Cell suspensions were incubated with dexamethasone, 10(-11)-10(-4)M, for 90 minutes at 37 degrees C. Rabbit beta-very low density lipoprotein(beta-VLDL) was obtained from New Zealand White rabbits that had been fed chow containing 1% cholesterol. Oxidative modification of beta-VLDL was performed by auto-oxidation. We measured the migration of monocytes in response to native and oxidized beta-VLDL using a 48-well microchemotaxis chamber. RESULTS: Oxidized beta-VLDL stimulated the migration of monocytes dose-dependently in the range between 0.5 and 2 nmol/mg protein. Dexamethasone inhibited the chemotaxis of monocytes exposed to oxidized beta-VLDL in a dose-dependent manner more than 10(-9)M. CONCLUSIONS: Inhibition of the chemotactic response of monocytes exposed to oxidized beta-VLDL may be a mechanism for the anti-atherogenic effect of dexamethasone in cholesterol-fed rabbits.

Animals↗
PubMed1992

Substrate-bound fibrinogen, fibrin and other cell attachment-promoting proteins as a scaffold for cultured vascular smooth muscle cells.

We have previously reported that fibrinogen/fibrin can induce the migration of vascular smooth muscle cells in vitro. In this study, we examined the effect of substrate-bound fibrinogen/fibrin and other cell attachment-promoting proteins on the adhesion of vascular smooth muscle cells. The amount of fibrinogen/fibrin adsorbed to plastic wells and the adhesion of smooth muscle cells to the wells were found to depend on the concentration of fibrinogen used for coating the wells. The effect of fibrinogen/fibrin was comparable to that of so-called cell attachment-promoting proteins (fibronectin, vitronectin, and type I collagen). Adhesion of smooth muscle cells to fibrinogen/fibrin-coated wells was inhibited by the synthetic peptide GRGDS, but not by a control peptide, GRGES. Vitronectin, fibronectin, type I collagen, denatured type I collagen and commercial gelatin also induced smooth muscle cell adhesion. The adhesion induced by vitronectin, denatured type I collagen, and commercial gelatin was inhibited by GRGDS. However, the adhesion induced by type I collagen was not influenced and that induced by fibronectin was only slightly inhibited. These observations suggest that fibrinogen/fibrin deposited extracellularly in the arterial intima may act as a scaffold in the process of smooth muscle cell migration.

Animals↗
PubMed1992

Nocturnal blood pressure monitored by ambulatory blood pressure measurement in elderly hypertensive patients.

This study was designed to characterize the nocturnal fall of blood pressure (NFBP) of elderly hypertensive patients (EH), with or without cerebrovascular disease or diabetes mellitus, as measured by automated blood pressure (BP) monitoring. Systolic and diastolic BP and heart rate was measured every 15 minutes in 133 hospitalized patients with nearly similar schedules and diets. The patients were divided into five groups: I, normotensive elderly patients over age 65: II, EH without cardiovascular diseases, controlled without medication: III, EH with cerebral infarction, chronic stage: IV, EH with noninsulin-dependent diabetes mellitus: and V, hypertensives under age 65, without cardiovascular diseases. A significant NFBP was observed in the patients of groups I and V, a significant but smaller NFBP in the hypertensives of groups II and IV, and no NFBP in the patients of group III. Administration of the antihypertensive drugs, enalapril and nifedipine, tended to augment the NFBP. These preliminary observations showed that NFBP did occur in elderly hypertensives but the fall was smaller than that observed in younger hypertensives or elderly normotensives. Although the ambulatory BP measurements were useful in the overall clinical evaluation of elderly patients, NFBP in elderly patients was affected by hypertensive drugs and therefore NFBP should be interpreted with caution.

Aged↗
PubMed1992

[Long-term nasogastric feeding and complications of acute gastric ulcer in two elderly patients].

Some elderly patients with chronic illness such as stroke, or Parkinsonism cannot take food orally because of dysphagia. In such cases, tube feeding can be used as a supplement to oral intake when malnutrition is present. This route allows for easier nursing care and decreases the frequency of aspiration pneumonia. Complications of tube feeding include nutrient deficiency states, pulmonary aspiration, gastrointestinal and metabolic disorders. We report two cases with complications of acute gastric ulcer which was thought to be induced with long-term tube feeding. Case 1 was a 61-year-old male patient with Parkinson's disease for ten years. L-DOPA had been administered with good control of his condition. However, his ability to swallow has deteriorated gradually. As he often suffered from aspiration pneumonia, nasogastric tube feeding was performed. After three years of tube feeding, he suddenly vomited much bloody material. He died from massive bleeding with acute gastric dilatation. Autopsy showed giant acute gastric ulcer covered with coagulated blood. UL3, 50 mm in maximum diameter, was observed in the middle portion of the greater curvature, where the top of tube probably came in contact with the gastric wall. Case 2 was an 83-year-old female patient with stroke and chronic heart failure. She had been hospitalized for about one year because of the intermittent deterioration of her cardiac condition. Furthermore, her inability to swallow increased during her hospitalization. She also suffered from aspiration pneumonia. Nasogastric tube feeding was performed to prevent aspiration pneumonia and malnutrition. She died of acute heart failure after twelve months. Autopsy revealed heart dilatation, old myocardial infarction and stroke. In addition, two acute gastric ulcers (UL3.10 and 30 mm in diameter) were recognized; one was in the upper portion of the greater curvature, the other in the lower portion of the greater curvature. The location of these gastric ulcers was unusual. Moreover, they coincided with location of top of the nasogastric tube. From these two cases, we conclude that in long-term tube feeding the tip of the tube often comes in contact with the gastric wall, and gastric ulcer could be produced by repeated mechanical stimulus of the wall. Reports of acute gastric ulcer induced by tube feeding have not been published previously. Therefore, we should pay much attention to this complication in the care of the elderly people with long-term tube feeding.

Acute Disease↗
PubMed1992

[Clinicopathological study of autopsy cases of pancreatic carcinoma in the elderly].

A total of 257 autopsy cases of pancreatic carcinoma, including 160 male and 97 female cases with an average age of 68.2 years, were divided into an aged group (70 years or older, 136 cases) and a control group (younger than 70 years, 121 cases), and their respective clinicopathological features were compared. The male to female ratio was 1.2:1 in the aged group and 2.6:1 in the control group. In both groups, abdominal pain was noted in about one-third of the cases as the primary symptom, followed by appetite loss and icterus. Concerning the primary symptoms, the two groups did not differ from each other. The rate of surgical resection was higher in the control group (24.0%) than the aged group (10.3%). Mean survival times were similar in both groups (5.71 months for the aged group and 6.01 for the control group). Intrapancreatic location of the tumor showed similar tendencies in both groups. However, cancer of the head of the pancreas was 2.3 times more common than body/tail cancer in cases aged 80 or more. Approximately 90% of the cases were diagnosed as ductal carcinoma by histological examination. The degree of differentiation was similar in both groups, but the well differentiated type was somewhat predominant in cases 80 years or older. Metastasis or direct invasion was noted to the liver, peritoneum and lung in this order in both groups. Liver and lymph node metastasis were less frequent in cases 80 years or older. Multiple primary cancers were noted in 8.8% of the aged group and 9.1% of the control.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

Effects of dexamethasone on experimental atherosclerosis in cholesterol-fed rabbits.

We studied the effects of a synthetic adrenocortical steroid, dexamethasone, on the development of experimental atherosclerosis in cholesterol-fed rabbits. Daily intramuscular injection of dexamethasone (0.125 mg/day) remarkably inhibited the aortic atherosclerosis induced by feeding a 1% cholesterol-rich diet for 8 weeks, although it aggravated diet-induced hyperlipidemia. Histologically, less foam cell accumulation was observed in the atherosclerotic lesions of the dexamethasone-treated rabbits as compared with the control animals. When rabbits were fed a normal chow diet for 10 weeks after receiving the 1% cholesterol-rich diet for 8 weeks, no regression of atherosclerotic lesions was observed with the daily injection of dexamethasone (0.125 mg/day); however, the drug again tended to inhibit further progression of atherosclerosis. The anti-atherogenic mechanism of dexamethasone may involve an inhibition of recruitment of blood monocytes and the insudation of atherogenic lipoproteins, mainly beta-very low density lipoprotein (beta-VLDL) in the present experiments, into the aortic intima, or it may involve a change in the size and structure of the lipoproteins, resulting in their decreased passage through the aortic endothelium into the intima.

Animals↗
PubMed1992

HDL does not promote cholesterol efflux from macrophages of hypercholesterolemic rabbit: efflux differences between species.

The purpose of this study was to investigate the difference between species (mouse and rabbit) and the effect of hypercholesterolemia on the ability of their peritoneal macrophages to release unesterified cholesterol to an exogenous acceptor. The macrophages from mouse, normocholesterolemic rabbits and hypercholesterolemic rabbits (Mm, Mnr, Mhr) were loaded with cholesterol esters by incubation with oxidatively modified low density lipoprotein or plasma lipoprotein (beta-migrating very low density lipoproteins). When human HDL was used as cholesterol acceptor for 24 h of incubation, the Mm Cells, the Mnr cells and Mhr cells retained about 40%, 70%, and more than 90% of their cholesterol esters. The difference between species of lipoproteins were not effective for the ability to release cholesterol esters. ACAT (acylcoenzyme A: cholesterol acyltransferase) inhibitor 58-035 increased these capacities. These data suggest that the limited capacity of macrophages from hypercholesterolemic rabbits to release cholesterol may be related to the progression and resistance to regression of atherosclerosis, and that ACAT activity might influence this capacity.

Animals↗
PubMed1990

[Nutrition in the elderly].

It is well known that nutrition plays an important role in the maintenance of health through the whole life. Especially, nutrition in the elderly is thought to be necessary for keeping their life comfortable. How much calories should be needed in the elderly? In our country, daily allowance of total calories is 1600 kcal in male and 1400 kcal in female in seventh decade respectively. 1460 kcal in male and 1270 kcal in female over eighty years old are recommended respectively. Protein requirement is about 0.6 g/kg of body weight. Fat should be kept as it is. Vitamin and mineral are the another important factors. We investigated the levels of serum vitamin B1 (B1) and B12 (B12) in 26 elderly out-patients. B1 and B12 are within normal ranges and there is no tendency to decline with age. Serum Zinc (Zn) is one of microelements and its deficiency is thought to cause the taste disorder. In 126 male subjects, Zn decreased significantly with aging. Zn correlated with serum total protein and albumin. There exists some discrepancy in the food habits between the old and the young: Dietary habits is Japanese style in the former and Western one in the latter. Recently as the old people are increasing in population, those who complain of difficulty in swallowing food are also increasing. In these cases, we should apply the artificial feeding such as central venous hyperalimentation, nasogastric and gastro-fistula feeding, etc. And ratio of these artificial food intake will increase in the near future.

Aged↗
PubMed1989

[Determination of serum lipid peroxidase using 10-N methylcarbamoyl-3,7-dimethylamino-10 H-phenothiazine (MCDP)--with special reference to aging and diseases].

We developed an assay for determining serum lipid peroxide (LPO) using MCDP. LPO levels in 125 healthy middle-aged and 70 elderly subjects. LPO level in the healthy and the elderly subjects was 1.45 +/- 1.37 nmol/ml and 2.1 +/- 3.0 nmol/ml, respectively. LPO did not increase with age. There was no correlation in the LPO levels determined by the MCDP and TBA methods. We determined the LPO distribution in the fractions of lipoprotein prepared by ultracentrifugation. In the LDL fraction of the diseased (myocardial infarction), the LPO level was higher than that of healthy subjects. Periodic measurement of LPO levels in 10 surgically operated patients revealed that the LPO level decreased significantly on the first day after operation. Our assay is easy to use and shows a lower level than the TBA method. LPO measured by this method would represent a substance different from that measured by the TBA method, i.e., MCDP mainly measures hydroperoxides, whereas the TBA method measures endoperoxides.

Animals↗
PubMed1987

Serum lipid peroxide assayed by a new colorimetric method.

Serum lipid peroxide (LPO) in 72 healthy male subjects was studied using a newly developed assay method based on the reaction of LPO with methylene blue derivative (MCDP; 10-N-Methylcarbamoyl-3,7-dimethylamino-10 H-phenothiazine). This method is specific for lipid hydroperoxide and the relation is equimolar. The value obtained was 7.63 +/- 2.78 nmol/ml. Positive correlations were observed between LPO and height (r = 0.290), body weight (r = 0.244) and hemoglobin (r = 0.248). However, no significant correlation was observed between serum LPO level and other clinical data, including age. In addition, serum LPO value measured by this method did not show significant correlation with that measured by the thiobarbituric acid method in rat serum. This discrepancy might be due to the differences in substrates measured by each method.

Adult↗
PubMed1984

Ineffectiveness of Ca2+-antagonists nicardipine and diltiazem on experimental atherosclerosis in cholesterol-fed rabbits.

There is accumulating evidence that calcium metabolism plays an important role in the pathogenesis of atherosclerosis. The inhibitory effect of nifedipine, a Ca2-antagonist, on experimental atherosclerosis in cholesterol-fed rabbits has been reported, and we examined the anti-atherosclerotic action of nicardipine and diltiazem, similar Ca2+-antagonists, but no inhibitory action was observed. It is necessary to recognize the fact that the sensitivity of rabbits to an anti-atherogenic diet shows great individual differences. For the purpose of preventing atherosclerosis due to the abnormality of lipid metabolism the use of Ca2+-antagonist is not warranted at the present stage.

Animals↗