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Biomedical subjects

M Tani

Publications and source records attributed to M Tani.

At least 325 records · Page 18Linked to original sources
PubMed1989

Atrial natriuretic factor (ANF) increases urinary protein excretion in patients with essential hypertension: a possible role of ANF for renal handling of protein.

Low dose iv infusion (0.01 and 0.03 micrograms/kg per min, for 30 min each) of alpha-human atrial natriuretic factor (alpha-hANF) produced a significant increase (+300%) in urinary protein excretion in patients with essential hypertension but not in normotensive controls, when their renal function was normal. The major component of excreted proteins induced by alpha-hANF infusion was presumed to be albumin on the basis of molecular weight (69,000) analyzed by sodium dodecyl sulfate (SDS)-polyacrylamide gel electrophoresis. Urine output and sodium and potassium excretion rates were increased dose-dependently by alpha-hANF infusion in the hypertensive patients in a similar fashion to those in the controls. Glomerular filtration rate (GFR) remained unchanged in the controls but was slightly increased in the patients (+33%) during the infusion. These results suggest that besides its previously recognized physiological functions such as natriuresis and diuresis, ANF plays an important role in the regulation of renal handling of proteins in patients with essential hypertension.

Adult↗
PubMed1989

Progressive restriction in the distribution of the Hox-1.3 homeodomain protein during embryogenesis.

Expression of the murine homeobox containing gene Hox-1.3 was analyzed in mouse embryos using polyclonal antisera to peptides predicted from cDNA and genomic sequences. At the earliest stage examined, 7.5 days gestation, cell nuclei throughout the three embryonic germ layers and in extraembryonic structures derived from the fertilized ovum were strongly immunoreactive. Rostro-caudal gradients or other patterns of regional differentiation in levels of expression could not be seen. Surrounding maternal tissue showed only weak immunoreactivity. At 8.5 days gestation, immunoreactivity was present in all embryonic structures including neural tube, somites and lateral plate mesoderm, ectoderm and endoderm. Immunoreactivity was progressively restricted thereafter. At 17 days gestation, strong immunoreactivity was largely restricted to the nervous system, both central and peripheral. Spinal cord was well stained, with a dramatic reduction in intensity near the junction of spinal cord and brain. In addition to this overall pattern, enhanced immunoreactivity appeared in limited populations of newly-formed neuroblasts of spinal cord and brain, suggesting that Hox-1.3 might serve to regulate the development of specific types of neurons following cessation of precursor cell mitosis.

Animals↗
PubMed1989

Role of interleukin-2 and interferon-gamma in induction of activated natural killer cells from mice primed in vivo and subsequently challenged in vitro with the streptococcal preparation OK432.

The natural-killer(NK)-cell-mediated cytotoxicity to syngeneic tumor cells can be augmented by in vivo priming and subsequent in vitro challenge with the streptococcal preparation OK432. Supernatants of cocultures of spleen cells with OK432 contained interleukin-2 (IL-2) and interferon (IFN), mainly IFN-gamma. As the anti-(mouse IFN-gamma) monoclonal antibody but not anti-(mouse IFN-alpha) antibody inhibited the induction of activated NK cells with OK432, the IFN-gamma participated in this response. The enhancement of NK cell activity and production of IL-2 were partially inhibited by the pretreatment of spleen cells with mitomycin C or irradiation, and were completely abolished by pretreatment with actinomycin D. The IL-2 activity after treatment with various metabolic inhibitors ran parallel to the NK activity in a system augmented with OK432. The activity of incubated spleen cells with IL-2 receptors was increased by OK432 treatment, and the NK cell and IFN activities of supernatants were also abrogated by the treatment with anti-(mouse IL-2 receptor) monoclonal antibody, to block the interaction between IL-2 and these receptors of effector cells. The panning method clarified that the incubated spleen cells with IL-2 receptors are responsible for the production of IFN-gamma. These results suggest that IL-2 plays a major role in inducing the activated NK cells from murine spleen cells primed in vivo and subsequently challenged in vitro with OK432, by the production of IFN-gamma.

Adjuvants, Immunologic↗
PubMed1989

Increased contact hypersensitivity response in mice by topical application of 1 alpha,25-dihydroxyvitamin D3 to elicitation site.

Recent evidence indicates that the biologically active metabolite of vitamin D3, 1 alpha,25-dihydroxyvitamin D3 [1 alpha,25(OH)2D3], has an effect on the regulation of the immune response. We investigated whether topical treatment of mice with 1 alpha,25(OH)2D3 influences the contact hypersensitivity (CHS) response to trinitrochlorobenzene (TNCB). 1 alpha,25(OH)2D3 was applied to the dorsal trunk of A/J mice on days 0-3, and on day 4 topical application of 5% TNCB on the 1 alpha,25(OH)2D3-treated site was performed. The mice were tested for CHS on day 10 by applying 1% TNCB to the ears. No effect on induction of CHS response to TNCB was observed in 1 alpha,25(OH)2D3-treated mice compared with 24,25-dihydroxyvitamin D3[24,25(OH)2D3]-treated mice as control. In a second experiment, the dorsal trunk of A/J mice was treated with 5% TNCB on day 0. The topical application of 1 alpha,25(OH)2D3 on the ears was performed from days 2 to 5. On day 6, the mice were tested for CHS by applying 1% TNCB to the 1 alpha,25(OH)2D3-treated ears. When 1 alpha,25(OH)2D3 was administered to the elicitation site prior to the challenge, pretreatment of mice with 1 alpha,25(OH)2D3 increased their response to TNCB by 40% compared with 24,25(OH)2D3-treated mice as control (P less than 0.01). There were no findings suggesting that the pretreatment of the challenge site with 1 alpha,25(OH)2D3 induced an irritant dermatitis that was superimposed on a subsequent CHS reaction. The 1 alpha,25(OH)2D3 modulation of CHS response to TNCB in mice suggests that the hormone may play a role in the regulation of the immune response in vivo.

Administration, Topical↗
PubMed1989

Bullous disease in systemic lupus erythematosus.

We describe three women with systemic lupus erythematosus and vesiculobullous skin lesions. One patient had a generalized bullous dermatosis and circulating anti-basement membrane zone IgG autoantibodies. Two patients had vesiculobullous lesions limited to the face. All patients had subepidermal blisters and an infiltrate of neutrophils and linear IgG, IgM, IgA, and C3 deposits along the basement membrane zone. These deposits were located in the sublamina densa. Ultrastructural investigation revealed a dermatolytic bullous disease in the patient with the generalized bullous eruption and anti-basement membrane zone autoantibodies and junctional blistering in those patients who had localized blistering.

Adult↗
PubMed1989

Pemphigoid nodularis.

A 61-year-old man with prurigo nodularis subsequently developed bullous pemphigoid. Direct immunofluorescence studies of a prurigo nodularis-like lesion and peribullous skin showed the deposition of IgG, IgA, and C3 in a linear pattern at the basement membrane zone. Indirect immunofluorescence studies disclosed circulating anti-basement membrane zone antibodies. Immunoelectron microscopy revealed IgG, IgA, and C3 distributed in the lamina lucida and on the undersurface of the basal keratinocytes in both peribullous and prurigo nodularis lesions. These findings confirmed the diagnosis of pemphigoid nodularis.

Complement C3↗
PubMed1989

Role of intracellular Na+ in Ca2+ overload and depressed recovery of ventricular function of reperfused ischemic rat hearts. Possible involvement of H+-Na+ and Na+-Ca2+ exchange.

The roles of H+-Na+ and Na+-Ca2+ exchange in the depression of ventricular function were studied in the reperfused isolated ischemic rat heart. Zero-flow global ischemia was induced for either 15 or 30 minutes and was followed by 30 minutes of aerobic reperfusion. Intracellular Na+ (Na+i) and 45Ca2+ uptake were measured during ischemia and reperfusion. Accumulation of Na+i was modified by prior glycogen depletion and by treatment with amiloride, a H+-Na+ exchange inhibitor, or monensin, a Na+ ionophore. Na+i rose continuously during ischemia and rapidly during the first two minutes of reperfusion. The larger inhibitory effect of amiloride and preischemic glycogen depletion was on Na+i accumulation during reperfusion; this finding suggests that the uptake occurs by H+-Na+ exchange. Reduction of Na+i accumulation by glycogen depletion was associated with less lactate and, presumably, H+ production and accumulation during ischemia. The rapid increase in Na+i during early reperfusion may reflect the readjustment of the low intracellular pH resulting from ischemia. The level of Na+i at the end of ischemia and especially after two minutes of reperfusion were linearly correlated with 45Ca2+ uptake and depression of ventricular function during subsequent reperfusion. This highly significant correlation between Na+i and 45Ca2+ uptake when Na+i was varied by several independent procedures, including monensin, strongly suggests that reperfusion 45Ca2+ uptake occurs at least in part by Na+-Ca2+ exchange. The rate of 45Ca2+ uptake during reperfusion was linearly and highly significantly correlated with elevation of diastolic pressure, reduced developed pressure, and decreased recovery of ventricular function. The data strongly support a mechanism of ischemic cell damage that involves excessive production and accumulation of H+ during ischemia that exchanges for extracellular Na+ during ischemia and rapidly during the first few minutes of reperfusion. Increased Na+i then causes excessive 45Ca2+ uptake and depressed recovery of cellular functions with continued reperfusion. Increased levels of Na+i may be a major event that couples a decreased intracellular pH during ischemia to excessive 45Ca2+ uptake and depressed recovery of cellular function with reperfusion.

Animals↗
PubMed1989

[Effects of scaling and root planing on clinical parameters and bacterial flora in periodontal pockets. 1. Changes in clinical parameters and subgingival bacterial flora after treatment].

The purpose of this study was to clinically and microbiologically evaluate the effects of supragingival plaque control, scaling and root planing on periodontal therapy. Six patients affected with moderate or severe periodontitis were selected. The clinical status of each patient was recorded with such clinical parameters as probing pocket depth (PD), probing attachment level (PAL), gingival crevicular fluid flow (GCF), gingival index (GI), gingival bleeding index (GBI), suppurative index (SI), and mobility (Mo). After the patients had learned to perform their own oral prophylaxis, they were treated by scaling and root planing. Microbiological status was assessed by phase contrast microscopy and bacterial forms were classified into following six groups: coccoid cells, rods, filaments, fusiforms, motile rods, spirochetes. The number and the relative proportion of each group were compared statistically. Clinical and microbiological status from baseline to 5 months after scaling and root planing were re-examined. The results obtained were as follows. 1. The most significant change in clinical and microbiological status was observed one month after scaling and root planing. In particular, the total number of the microorganisms and the number and relative proportion of motile organisms were reduced. 2. Thereafter clinical and microbiological status was maintained during experimental period by means of supragingival plaque control.

Dental Plaque↗
PubMed1989

[Effects of scaling and root planing on clinical parameters and bacterial flora in periodontal pockets. 2. Correlation between decrease of probing pocket depth and pretreatment status].

Scaling and root planing is one of the most fundamental and effective procedures in periodontal therapy. The purpose of this study was to investigate statistically whether clinical or microbiological parameters before treatment are related to changes in probing pocket depth (PD). Two kinds of numerical values represented changes in PD. One was pocket difference (A-B: A; PD before the treatment and B; PD after treatment) and the other was rate of pocket decrase [(A-B)/A x 100]. Twenty four sites in six patients with periodontal pockets deeper than 4 mm were selected for this study. Clinical parameters such as PD, probing attachment level (PAL), gingival crevicular fluid (GCF) volume, gingival bleeding index (GBI) and suppurative index (SI) were recorded at each site. Subgingival plaques sampled at the same site were evaluated by phase contrast microscopy. The results obtained were as follows: 1. Of all the clinical parameters changes in PD were most positively correlated with PD before treatment. 2. The microbiological approach revealed that total bacterial count divided by PD value was more negatively correlated with changes in PD than total bacterial number. It was further, revealed that numbers of rods and motile bacteria were more closely correlated with changes in PD than the counts of bacterial groups. At sites where coccoid cells were relatively dominant, PD tended to decrease readily. Motile bacteria, on the other hand, exhibited just the opposite relationship. These results suggest that periodontal treatment should be more effective in periodontal pockets harboring both smaller numbers of rods and motile bacteria.

Dental Scaling↗
PubMed1989

[Sinus node function evaluated by spontaneous atrial premature contractions].

Sinus node function was evaluated according to spontaneous premature atrial contractions (APC). In 33 patients, who showed evidence of more than 10 APCs in 24-hour Holter ECG, sinoatrial conduction times (SACT) were measured by the Strauss' method. Time difference between the interval preceding PP, the APC and return cycle following APC was expressed as RC-SC. Patients were categorized in three groups; CSRT less than 500 and 2SACT less than 180 msec (A), 500 less than or equal to CSRT less than 1000 and/or 180 less than or equal to 2SACT less than 250 msec (B), and CSRT greater than or equal to 1000 and or 2SACT greater than or equal to 250 msec (C). There was significant correlation between the mean RC-SC and 2SACT (r = 0.69). Mean RC-SC was greater than 2SACT in all seven patients whose CSRTs exceeded 2000 msec. The mean RC-SC was 0.15 +/- 0.03 in group A, 0.20 +/- 0.02 in group B and 0.25 +/- 0.06 (sec; mean +/- SD) in group C. The max RC-SC was 0.20 +/- 0.03 in group A, 0.28 +/- 0.03 in group B and 0.36 +/- 0.07 sec in group C. The mean RC-SC and max RC-SC differed significantly among the three groups (p less than 0.05). The standard deviation in distribution of the RC-SC was 0.033 +/- 0.008 in group A, 0.044 +/- 0.007 in group B and 0.052 +/- 0.017 sec in group C. RC-SCs equal to or longer than 0.24 sec were observed in 1% in group A, 26% in group B and 58% in group C, and that equal to or longer than 0.30 sec was found in 0, 3 and 28% in groups A, B and C, respectively. The RC-SC reflects not only SACT but sinus node automaticity, and provides more simple detection of sinus dysfunction. Sinus dysfunction may exist when the RC-SC is greater than 0.30 sec.

Adult↗
PubMed1989

Atrial natriuretic peptide in human neuroblastoma.

To clarify the presence of atrial natriuretic peptide (ANP) in neural tissue, extracts from human neuroblastoma which is considered of neural crest origin were analyzed using a specific radioimmunoassay (RIA) for ANP. High concentrations of immunoreactive ANP ranging from 2.7 to 18.4 ng per mg of protein were demonstrated in the tissue. Furthermore, high performance gel permeation chromatography (HPGPC) coupled with the RIA revealed that the immunoreactive ANP found in the tissue consisted of only one component with molecular weight of 12,000 to 13,000 daltons, corresponding to gamma-human ANP (hANP). These results could be direct evidence for generation of ANP intrinsic of human neuronal tissue, and also suggest that neuroblastoma can be used as a model for investigation of mechanism of ANP formation within the neuronal tissues.

Atrial Natriuretic Factor↗
PubMed1989

[Incessant supraventricular tachycardia due to upper atrioventricular nodal reentry].

Three patients with recurrent supraventricular tachycardia were presented. Atrial cycle length unchanged during the tachycardia with antegrade Wenckebach AH block was observed. When AH block occurred during tachycardia, the first AH interval was shorter than the subsequent one. The tachycardia was initiated and terminated by atrial extrastimulation beyond the atrial relative refractory period and the atrial activation sequence during the tachycardia was low to high. The induction of tachycardia was dependent on a critical AH interval. Ventriculoatrial conduction was not observed in patient 1 and 2. In patient 3 who had ventriculoatrial conduction, the tachycardia was initiated by the premature ventricular stimulation followed by double atrial response, and the tachycardia was terminated by the ventricular stimulation without atrial capture. In patient 1, verapamil (5 mg) prolonged the atrial cycle length during tachycardia and rapid intravenous injection of adenosine triphosphate (10 mg) terminated the tachycardia. Oral diltiazem (180 mg/day) suppressed the tachycardia in patients 2 and 3. These findings suggest that the mechanism of the tachycardia may be fast-slow type of AV nodal reentry in the upper portion of the AV node and this type of arrhythmia has a tendency to be incessant.

Adenosine Triphosphate↗
PubMed1988

Intermittent Wolff-Parkinson-White syndrome due to phase 3 and phase 4 block: disappearance of rapid ventricular response during atrial fibrillation.

A 65-year-old man with Wolff-Parkinson-White syndrome type A had a rapid ventricular response over an accessory pathway during atrial fibrillation. Four months later, electrophysiological study revealed the following properties: 1) The antegrade accessory pathway conduction showed phase 3 and phase 4 block. 2) The retrograde concealed accessory pathway conduction eliminated phase 4 block in the antegrade accessory pathway conduction. 3) Premature ventricular excitation arose from the accessory pathway or from the ventricular muscle close to its distal end. 4) Atrial fibrillation during isoproterenol infusion did not show rapid ventricular response. Spontaneous impairment of accessory pathway conduction due to phase 3 and phase 4 block was suspected.

Aged↗
PubMed1988

Hearts from diabetic rats are more resistant to in vitro ischemia: possible role of altered Ca2+ metabolism.

The effects of whole heart ischemia were studied in isolated perfused rat hearts from control and diabetic animals. When whole heart ischemia was maintained for 30 minutes at 37 degrees C, diabetic hearts recovered 100% whereas hearts from normal animals recovered 30% of their preischemic function. Reperfusion Ca2+ uptake was about 2.5 microM/g dry wt in diabetic hearts compared with 10 microM/g dry wt in control hearts. When the ischemic period was extended to 40, 50, and 60 minutes, diabetic hearts had depressed recovery of ventricular function, and greater Ca2+ overload but reperfusion function was still significantly higher and Ca2+ overload significantly less than in control hearts. Depressed function and increased Ca2+ uptake were both linearly related to low tissue levels of residual high energy phosphates and inversely related to the amount of lactate that accumulated in the tissue during ischemia. However, regression lines relating these metabolic changes to depressed function and increased Ca2+ uptake showed that for any level of residual high energy phosphate or ischemic lactate, diabetic hearts performed much better and had less Ca2+ uptake than control hearts. These effects of diabetes were due to the diabetogenic action of the drugs used since both streptozotocin and alloxan had the same effect and in vivo insulin treatment reversed the effect. Diabetic hearts had a reduced maximum inotropic effect to increased extracellular Ca2+ under control aerobic perfusion conditions. The improved recovery of ventricular function during reperfusion of ischemic hearts from diabetic animals was highly correlated with reduced Ca2+ uptake, and regression lines relating depressed ventricular function to Ca2+ overload showed that data from control and diabetic hearts fell on the same line; that is, when depressed function occurred it was related to increased Ca2+ uptake to the same extent in both control and diabetic hearts. The resistance to ischemia in diabetic hearts was not related to higher tissue levels of high energy phosphates during reperfusion nor to lactate accumulation during ischemia. The observations suggest a role of increased reperfusion Ca2+ influx in ischemic damage and that alterations of sarcolemmal Ca2+ transport systems in diabetic myocardium may account for the greater resistance of these hearts to ischemia.

Animals↗