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Biomedical subjects

T Shoji

Publications and source records attributed to T Shoji.

At least 127 records · Page 7Linked to original sources

Long-term recording of olfactory and vomeronasal stimulant-induced waves from the turtle main olfactory bulb and accessory olfactory bulb.

Recording of stimulant-induced waves (bulbar responses) from the main olfactory bulb is a useful tool for measuring quantitative stable olfactory responses. There is a good relationship between the olfactory bulbar response, olfactory nerve response and electroolfactogram (EOG), suggesting that the bulbar response reflects events in receptor cells. The modern whole-cell recording technique offers direct information on olfactory transduction in single cells, but it requires long experimental periods and many animals. On the other hand, analysis of bulbar responses provides useful information and requires the use of few animals. For example, we found that cAMP-increasing and IP3-increasing odorants were not distinctly received by the turtle olfactory organ by measuring olfactory bulbar responses and analyzed with a multidimensional scaling from about 60 animals. However, to record similar odor responses from isolated turtle olfactory neurons, at least 200 animals would be necessary. Bulbar responses are recorded with electrodes implanted into or located on the main olfactory bulb. When electrodes are located on the olfactory bulb surface, it is possible to record stable responses over a period of 3 days. These methods were applied successfully to the accessory olfactory bulb. In this paper, we describe the protocols used for recording of the stimulant-induced waves from the main and accessory olfactory bulb.

Adaptation, Physiological↗

A novel protein with DNA binding activity from tobacco chloroplast nucleoids.

A 41-kD DNA binding protein with a basic pl was purified from chloroplast nucleoids in photomixotrophically cultured tobacco cells, and its amino acid sequence was determined. Using this sequence information, its cDNA (CND41) was isolated, and its nucleotide sequence was determined. The predicted amino acid sequence of CND41 has a transit peptide of 120 amino acids and a mature protein of 382 amino acids. A distinctive helix-turn-helix motif in the lysine-rich N-terminal region of the mature protein and an aspartyl protease active site motif were predicted. Expression of a series of truncated CND41 proteins in Escherichia coli indicated that the lysine-rich region is essential for DNA binding and that CND41 nonspecifically binds chloroplast DNA. Protein gel blot analyses showed CND41 mainly in cells and/or tissues containing nonphotosynthesizing, actively growing plastids. In addition, the accumulation of chloroplast transcripts in these cells and/or tissues (e.g., transcripts for QB binding protein of photosystem II [psbA] and large subunit of ribulose bisphosphate carboxylase [rbcL]) was negatively correlated with the accumulation of CND41. Analyses of cultured cells of transgenic tobacco with reduced CND41 levels showed a higher level of expression of chloroplast genes compared with that of the wild type. We discuss the possible function of CND41 as a negative regulator of chloroplast gene expression.

Amino Acid Sequence↗

Progressive effects of phloridzin on melanogenesis in B16 mouse melanoma cells.

When we studied the effects of polyphenols from apple fruits on melanogenesis in B16 mouse melanoma cell lines, phloridzin had dose-dependent progressive effects on melanogenesis between 10 and 500 micrograms/ml without inhibiting cell growth. At a concentration of 500 micrograms/ml, phloridzin increased the melanin content in the cells to 181% of that in control cells. In contrast, phloretin, the aglycon of phloridzin, did not activate melanogenesis in the cells and was cytotoxic at a concentration of 5 micrograms/ml. Phloridzin increased the activity of tyrosinase to 223% of that in control cells. Furthermore, phloridzin inhibited the activity of protein kinase C (PKC), which is recognized to regulate tyrosinase activity. The inhibition of PKC activity continued for 120 min from the addition of phloridzin. Therefore, we estimated that the activation of melanogenesis by phloridzin resulted from the increase of tyrosinase activity caused by the inhibition of PKC activity.

Animals↗

Effect of polymorphism of apolipoprotein E and angiotensin-converting enzyme genes on arterial wall thickness.

We examined the association between the polymorphism of the apolipoprotein E (apoE) and the ACE genes and the intima-media thickness (IMT) of the carotid and femoral arteries measured using ultrasonography. The values of IMT of each artery were significantly higher in NIDDM patients (n = 356) than in control subjects (n = 235). The E4 allele or the D allele did not affect clinical characteristics, including age, fasting plasma glucose, total cholesterol, HDL cholesterol, LDL cholesterol, or blood pressure, in NIDDM or control subjects. No difference in the carotid IMT value was noted among the apoE genotypes in control or diabetic subjects. The carotid IMT was significantly higher in diabetic patients with the DD genotype (1.200 +/- 0.586 mm) than in those with the II genotypes (0.990 +/- 0.364 mm). Neither the E4 allele nor the D allele affected the femoral IMT in control or diabetic subjects. Multiple regression analysis demonstrated that the carotid IMT of NIDDM patients was associated with age, the D allele, and LDL cholesterol but not with the E4 allele, whereas that of control subjects was associated with age, sex, systolic blood pressure, LDL cholesterol, and HDL cholesterol, inversely. These results suggested that the E4 allele was not associated with the carotid or femoral IMTs, but that the D allele was statistically associated with carotid IMT in NIDDM patients but not control subjects. However, since the association was weak (2.3% explanatory power), its biological significance remains to be determined.

Adolescent↗

[Long-term follow-up study of bone mineral density in a patient with adult idiopathic Fanconi syndrome].

A 64-year-old woman complaining of severe lumbar pain was admitted to our hospital because of the finding of pre-existing mitral valve regurgitation on examination. Laboratory data revealed the proximal type of renal tubular acidosis, renal glucosuria, phosphaturia, generalized aminoaciduria and low-molecular-weight proteinuria. She did not have any cause of these tubular dysfunctions, and was diagnosed as adult idiopathic Fanconi syndrome. Dual energy X-ray absorptiometry (DEXA) revealed a reduction of bone mineral density in the lumbar spine to about 65% of the age-and gender-matched control value. Alkali agents (sodium citrate and potassium citrate), calcium lactate and 1 alpha-hydroxyvitamin D3 were administered. Bone mineral density estimated with DEXA improved with a reduction of serum alkali phosphate and disappearance of lumbar pain, and was restored to 82% of the age-and gender-matched control value after about 30 months of treatment. DEXA is useful for the long-term follow-up study of bone mineral density in a patient with Fanconi syndrome.

Absorptiometry, Photon↗

[Demonstration of heat shock protein, ubiquitin, in fire death autopsy cases by immunohistochemical study].

The expression of ubiquitin in heart, lung, liver, kidney and adrenal gland, was immunohistochemically studied in 23 autopsy cases died by fire accident. There were no correlations between the localization of ubiquitin in each organ, and burn extent, and burn degree, and carboxyhemoglobin (COHb) saturation. In serious tracheal burn cases, strong immunoreactivities of ubiquitin were observed in the lung. On the other hand, in cases of high concentration of cyanide, the ubiquitin immunostaining in the lungs was weak. These results indicate that in fire death cases, the expression of ubiquitin is affected by cyanide. In many cases strong immunoreactivities of ubiquitin were found in the adrenal glands, suggesting that the adrenal gland reacts strongly to the heat shock. Only three out of 23 autopsy cases showed the negative staining of ubiquitin immunoreactivity. Probably this is resulted from the early death prior to the expression of ubiquitin.

Adrenal Glands↗

Eruptive melanocytic nevi after Stevens-Johnson syndrome.

Widespread melanocytic nevi may rarely appear suddenly after a severe bullous disease. We describe two patients in whom eruptive melanocytic nevi developed 3 weeks after a severe episode of Stevens-Johnson syndrome. Benign melanocytic proliferation may develop after a bullous dermatosis and should not be confused with malignant or metastatic melanoma.

Adolescent↗

Atherosclerosis in uremia: possible roles of hyperparathyroidism and intermediate density lipoprotein accumulation.

Cardiovascular motality is high in patients with chronic renal failure treated with dialysis, and secondary hyperparathyroidism may promote atherosclerogenesis. Recent studies have revealed advanced atherosclerosis in hemodialysis patients by using high-resolution B-mode ultrasonography. Multiple regression analyses indicated that hyperphosphatemia and hyperparathyroidism were associated with increased intima-media thickness (IMT) of the carotid and femoral arteries in hemodialysis patients, respectively. Hypocalcemia and hyperparathyroidism independently and adversely affect the lipoprotein profile by suppressing hepatic triglyceride lipase (HTGL), a lipid-regulating enzyme playing important roles in the metabolism of intermediate density lipoprotein (IDL) and high density lipoprotein (HDL). Plasma IDL is raised markedly, and HDL is lowered in uremia. These lipoprotein changes are closely associated with increased aortic pulse wave velocity (PWV), an index of aortic sclerosis. These findings support the hypothesis that deranged calcium-phosphate homeostasis and secondary hyperparathyroidism promote atherosclerosis in uremia, at least partly by affecting lipoprotein metabolism. Adequate dialysis and efforts to normalize calcium, phosphate and PTH would be beneficial in preventing not only bone disease, but atherosclerosis as well.

Adult↗

[Mechanism mediating hypertension induced by chronic inhibition of nitric oxide synthesis].

Although the inhibition of nitric oxide (NO) synthesis is known to induce systemic hypertension, the underlying mechanisms mediating this type of hypertension are incompletely understood. In the present study we investigated the influence of sodium intake on the pressor effect of long-term administration of the NO synthesis inhibitor, NG-nitro-L-arginine methyl ester (L-NAME, 16 mg/dl in drinking fluid for 8 weeks), in conscious Sprague-Dawley rats. Urinary excretion rates of catecholamine during NO synthesis inhibition were also examined. Long-term administration of L-NAME produced a sustained elevation in tail-cuff pressure without altering urine flow, or sodium excretion rate. L-NAME-induced hypertension was accompanied by a decreased urinary excretion of the stable NO metabolites, NO2- and NO3-, and was aggravated when rats drank 0.9% saline in place of tap water. Thus, inhibition of NO synthesis resulted in a rightward shift of the pressure natriuresis relationship and a significant decrease in the slope of this relationship. Urinary excretion of epinephrine and norepinephrine, but not that of dopamine, in L-NAME-treated rats significantly increased within the first week of the study when compared with those observed in control rats. A natriuretic index of the sympathetic nervous system, the ratio of dopamine to norepinephrine excretion, was significantly less in L-NAME-treated rats than in control rats. After 8-week treatment with L-NAME, renal morphologic evaluation revealed significant narrowing and obliteration of the arterioles. L-arginine (2 g/dl in drinking fluid) completely reversed the elevation of blood pressure as well as the decrease in urinary NO2- and NO3- excretion and the increased urinary excretion of catecholamines associated with L-NAME treatment after 3 weeks of concomitant administration. These results suggest that the inhibition of chronic NO synthesis produces sodium-sensitive hypertension and that changes in sympathetic nerve activity may, at least in part, contribute to the sodium sensitivity in this type of hypertension.

Animals↗

Angiotensin-converting enzyme gene polymorphism is associated with carotid arterial wall thickness in non-insulin-dependent diabetic patients.

BACKGROUND: The insertion/deletion (I/D) polymorphism of the ACE gene has been shown to be associated with cardiovascular disease in healthy subjects as well as in patients with non-insulin-dependent diabetes mellitus (NIDDM). We investigated the relationship between the ACE gene polymorphism and the wall thickness of both carotid and femoral arteries in NIDDM patients. METHODS AND RESULTS: We measured the intimal plus medial thickness (IMT) of both carotid and femoral arteries using high-resolution B-mode ultrasonography in 288 Japanese NIDDM patients (160 men, 128 women). No significant differences among the three genotypes were found with respect to age, sex, duration of diabetes, body mass index, blood pressure, plasma glucose, hemoglobin AIC, total cholesterol, triglycerides, HDL cholesterol, or cigarette-years. Plasma ACE levels were strongly associated with I/D polymorphism, with an additive effect of the D alleles. The carotid IMT of the patients carrying the D allele (DD+ID genotype) was significantly higher than that of the patients not carrying the D allele (II genotype) (P = .037), whereas the femoral IMT was not affected by the I/D polymorphism. Multiple regression analysis demonstrated that the risk factors for carotid IMT of patients with NIDDM were age, non-HDL cholesterol, and D allele of the ACE gene (R2 = .155, P < .0001). CONCLUSIONS: The D allele of the ACE gene may be a risk factor for the development of wall thickening of the carotid but not the femoral artery in NIDDM patients.

Adolescent↗

Atrial activation during chronic atrial fibrillation in patients with isolated mitral valve disease.

BACKGROUND: A computerized 32-channel mapping system has been developed to investigate the characteristics of the atrial activation sequence. The system is capable of displaying sequential atrial maps and provides a rapid and dynamic means of verifying the activation sequence of atrial fibrillation. METHODS: Using this system, we performed intraoperative atrial activation mapping in 10 patients with chronic atrial fibrillation who were undergoing isolated mitral valve operations. RESULTS: Regular and repetitive activation (cycle length ranged from 131 to 228 milliseconds) originated in the left atrium in all 10 patients. Two patterns of repetitive activation in 2 patients and three patterns in 1 patient appeared alternately during the observation period in the left atrium. In contrast to the repetitive activation in the left atrium, the activation sequence of the right atrium was extremely complex and chaotic. In 7 of the 10 patients, the same pattern of right atrial activation was never repeated during the observation period. In 2 patients, revolution of repetitive activation in the right atrium sporadically appeared, but the pattern of activation immediately deteriorated to a complex and chaotic pattern. In 1 patient, repetitive activation emerged from the low lateral portion of the right atrium. Because our mapping technique was limited by the number of available atrial electrodes, discrete reentrant circuits or ectopic foci could not be demonstrated in the present study. However, the activation sequences during chronic atrial fibrillation suggested that (1) the left atrium would act as an electrical driving chamber for atrial fibrillation in the majority of the patients and (2) atrial activation patterns are different in each case. CONCLUSIONS: Computerized intraoperative mapping should guide surgeons in determining the appropriate surgical procedure and facilitate operation for chronic atrial fibrillation associated with mitral valve disease.

Adult↗

Comparative cytogenetic studies of benign, borderline, and malignant epithelial ovarian tumors.

Comparative cytogenetic studies were performed in 40 cases of untreated epithelial ovarian tumors. Of these 40 tumors, 13 were classified as benign, 3 as borderline, and 24 as malignant, according to the WHO classification for ovarian tumors. Of 13 benign ovarian tumors, 4 (30.8%) showed chromosomal abnormalities. Of 4 ovarian tumors, 3 (75%) had single chromosomal abnormalities, and the remaining tumor (25%) retained multiple chromosomal abnormalities. Of 3 borderline-malignant ovarian tumors, 2 (66.7%) showed chromosomal abnormalities. Of 2 ovarian tumors, 1 (50%) indicated single chromosomal abnormalities, and the remaining tumor (50%) revealed multiple chromosomal abnormalities. Of 24 malignant ovarian tumors, 20 (83.3%) showed chromosomal abnormalities. Of these 20 ovarian tumors, 3 (15%) had single chromosomal abnormalities, and the other 17 (85%) exhibited multiple chromosomal abnormalities. These data indicate that the rate of chromosomal abnormalities, especially multiple abnormalities, increases following the progression of malignancy in epithelial ovarian tumors.

Adenoma↗

Antineutrophil cytoplasmic antibodies (ANCA)-associated crescentic glomerulonephritis and propylthiouracil therapy.

Cutaneous vasculitis is an uncommon complication of propylthiouracil therapy. Although its pathogenesis remains to be established, detection of antineutrophil cytoplasmic antibodies (ANCA) in association with this type of vasculitis has recently been described. We report here 2 patients who developed ANCA-associated crescentic glomerulonephritis without evidence of cutaneous vasculitis during propylthiouracil treatment of hyperthyroidism. Improvement of the renal function and the disappearance of ANCA were correlately found after discontinuation of propylthiouracil and by corticosteroid therapy in both patients.

Adult↗

Olfactory responses of a euryhaline fish, the rainbow trout: adaptation of olfactory receptors to sea water and salt-dependence of their responses to amino acids

Salmonid fishes are able to survive in both fresh water and sea water. Concentrations of NaCl in fresh water and sea water are 0.5 and 493 mmol l-1, respectively, and, hence, salt concentrations in the medium at the olfactory epithelium are greatly changed when the fish migrate between fresh water and sea water. We used the rainbow trout, which is a salmonid fish, to examine the adaptation mechanisms of the olfactory receptors to high concentrations of salts in sea water. Application of sea water to the olfactory epithelium elicited only a very small response in the olfactory nerve, but 500 mmol l-1 NaCl elicited a large response which did not adapt to a spontaneous level with time. It is considered that the olfactory nerve becomes fatigued when the olfactory epithelium is exposed to 500 mmol l-1 NaCl for long periods. We found that the presence of 10 mmol l-1 Ca2+ in sea water inhibited the response to 500 mmol l-1 NaCl, suggesting that Ca2+ in sea water is essential for adaptation of the olfactory receptors to sea water. In the second part of the study, we examined whether the olfactory nerve responses to amino acids, potent stimulants for fish, were altered between fresh water and sea water. The magnitudes of the responses to the six amino acids examined were similar in artificial pond water and artificial sea water, indicating that a large change in NaCl concentration between fresh and sea water does not affect the olfactory nerve responses to amino acids. We used fish reared in fresh water and fish acclimated to sea water and obtained similar results. It was concluded that the tolerance of the olfactory receptors for large changes in osmotic pressure is not acquired while fish are maintained in fresh or sea water, but that the receptors of these euryhaline fish naturally provide the tolerance.

Journal Article↗

A case report of simultaneous surgery for Wolff-Parkinson-White syndrome combined with hemolytic anemia and mitral stenosis.

A 46-year-old woman with mitral stenosis, WPW syndrome, hemolytic anemia due to spherocytosis, and hypothyroidism with Hashimoto's thyroiditis, was admitted with palpitations and dyspnea due to paroxysmal atrial fibrillation with a rapid ventricular response, and was treated by electrical cardioversion. We selected surgical intervention to treat the mitral stenosis and WPW syndrome, as some tachycardia episodes due to atrial fibrillation have resulted in repeated congestive heart failure. In 1983 we simultaneously performed a division of the posteroseptal accessory pathway and a mitral valve replacement with a bioprosthetic valve under cardiopulmonary bypass, using a membrane oxygenator after splenectomy to compensate for the hemolytic anemia due to spherocytosis. Her postoperative course was favorable and she is now in good health with no episodes of tachycardia, congestive heart failure nor anemia occurring during the 10 years that have followed the operation. Simultaneous surgery for WPW syndrome combined with other cardiac abnormalities and hematologic disorders achieved acceptable results in this case.

Anemia, Hemolytic↗