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T Oka

Publications and source records attributed to T Oka.

At least 577 records · Page 32Linked to original sources

Converting enzyme inhibition improves congestion and survival in hypertensive rats with high-output heart failure.

The effects of angiotensin-converting enzyme (ACE) inhibitors in high-output heart failure have not yet been well established. We evaluated the effects of lisinopril (3 mg/kg/day) on hemodynamics, neurohormones, and survival in 10-week-old spontaneously hypertensive rats (SHR) with aortocaval fistula. Sham-operated treated and untreated SHR served as controls. Cardiac output (CO) was determined by thermodilution method, and renal blood flow (RBF) was assessed by laser-Doppler flowmetry. In sham-operated SHR, 2-week treatment with lisinopril decreased blood pressure (BP), left ventricular (LV) weight, and total peripheral resistance (TPR) (p < 0.01 each) and increased RBF and plasma renin activity (PRA) (both p < 0.05); CO and LV end-diastolic pressure (LVEDP) were unchanged. Fistula creation induced biventricular hypertrophy and high-output heart failure [increased LVEDP, CO, pulse pressure, and plasma norepinephrine (NE) and decreased RBF] with congestive signs (ascites, tachypnea). Lisinopril decreased LVEDP (p < 0.01), increased RBF, prolonged survival (both p < 0.05), and prevented ascites (0 vs. 46%) and increased PRA (p < 0.05) and attenuated the increase in plasma NE. Heart weight, BP, and CO were not affected by lisinopril. Thus, lisinopril ameliorated congestion and improved survival in SHR with fistula without compromising cardiorenal hemodynamics. Venous and renal dilatation and attenuation of vasoconstrictive systems may have contributed to the beneficial effects.

Animals↗

Rearrangement of bcl-2 is detectable in Hodgkin's disease by polymerase chain reaction.

The authors examined the occurrence of the t(14;18) chromosomal translocation in 44 cases of Hodgkin's disease (HD) using the polymerase chain reaction and Southern blot hybridization with non-radioactive oligonucleotide probes. DNAs were extracted from unfixed, fresh-frozen and formalin-fixed, paraffin-embedded biopsy specimens. Southern blot hybridization of the amplification product showed that, of 44 HD DNAs, three had a detectable t(14;18) breakpoint at the mbr (major breakpoint region), while none had a detectable t(14;18) breakpoint at the mcr (minor cluster region). Of the three cases positive for a t(14;18) breakpoint at the mbr, two were of lymphocyte predominance type, and the other was of mixed cellularity type.

Apoptosis↗

Giant cell tumor of the lung: an autopsy case report with immunohistochemical observations.

Tumors resembling giant cell tumor (GCT) of bone are well known to occur in other organs and many cases have been reported to date. While GCT occurring as primary lesions in the lung are extremely rare, the authors experienced such a tumor at an autopsy of a 77 year old woman and subsequently performed histological and immunohistochemical examinations. The clinical and morphologic characteristics of this case are documented, and the literature concerning this type of tumor is reviewed. The present tumor of the lung was histologically characterized by proliferation of benign-looking osteoclast-like giant cells in association with slightly atypical mononuclear cells. The tumor cells were immunohistochemically positive for histiocytic markers but negative for epithelial markers. This case appears to be the first reported benign giant cell tumor of the lung in which histiocytic differentiation of mononuclear cells was suggested by immunohistochemistry.

Aged↗

Progesterone and EGF inhibit mouse mammary gland prolactin receptor and beta-casein gene expression.

Regulation of mouse mammary gland long-form prolactin receptor (PRL-RL) mRNA levels by progesterone and epidermal growth factor (EGF) and the relationship between PRL-RL and beta-casein gene expression were examined in vivo and in vitro. PRL-RL and beta-casein mRNA levels increased approximately 6- and 15-fold from the pregnant to the lactating period, respectively, when normalized to the level of beta-actin mRNA. Ovariectomy of pregnant mice rapidly reduced the serum concentration of progesterone and increased the level of PRL-RL and beta-casein mRNAs approximately three- and fourfold compared with sham-operated animals 24 h after the operation. Injection of progesterone, but not estrogen, inhibited the increase in both mRNA levels. PRL-RL and beta-casein mRNA levels in cultured mammary epithelium increased in response to insulin, hydrocortisone, and prolactin, whereas progesterone or EGF caused inhibition. The combination of EGF and progesterone produced a greater inhibition than either hormone alone. These results indicate that both progesterone and EGF serve as negative regulators of lactogenesis.

Animals↗

EP1-receptor mediation of prostaglandin E2-induced hyperthermia in rats.

To investigate what type of prostanoid receptors are involved in the development of fever induced by brain prostaglandin E2 (PGE2), PGE2 and its analogues were injected into a lateral cerebroventricle (LCV) of rats, and the changes in colonic temperature (Tco) were observed in a 23 +/- 1 degrees C environment. 17-Phenyl-omega-trinor-PGE2 (an EP1 agonist; 0.01-10 nmol) produced a rapid and dose-dependent rise in Tco. Even though the EP1 agonist was 10 times less potent than PGE2 on a molar basis, the time course of this hyperthermia was quite similar to that of the PGE2-induced one. No fever was elicited by an LCV injection of butaprost (an EP2 agonist; 0.1-100 nmol), 11-deoxy-PGE1 (an EP2 agonist; 0.1-1.0 nmol). The PGE2 (0.3 nmol)-induced hyperthermia was blocked by LCV pretreatment with SC-19220 (150 nmol), an EP1 antagonist. The results suggest that the PGE2-induced hyperthermia in the rat is mediated predominantly through EP1 receptors in the brain.

Alprostadil↗

Light microscopical immunohistochemical study on parathyroid adenoma in primary hyperparathyroidism.

Fifteen adenomatous parathyroid glands obtained from 15 patients with primary hyperparathyroidism were examined both pathologically and immunohistochemically and connected with the clinical data for each patient. Four consecutive sections of the largest section surface of each resected adenomatous parathyroid gland were utilized for 4 kinds of stains, that is, hematoxylin-eosin, Grimelius and the immunohistochemical stains for parathyroid hormone (PTH) and chromogranin A. The results were as follows: (1) The large adenomatous parathyroid glands showed strong reactions to PTH as well as chromogranin A and Grimelius. On the other hand, the parathyroid adenoma obtained from a 9-year-old boy with hypercalcemic crisis showed almost no stain-positive cells for both PTH and chromogranin A. It is assumed that the former phenomenon reflects a substantial storage of secretory granules, while the latter reflects exhaustion of these granules. (2) The normal parathyroid cells in the neoplastic parathyroid glands generally showed stronger reactions to PTH and chromogranin A than neoplastic parathyroid cells. This suggests that normal cells in the neoplastic parathyroid glands may have their release of PTH rather than its synthesis suppressed, and also might support the hypothesis of some authors that chromogranin A or SP-I might contribute to stabilization of PTH or the secretory vesicle.

Adenoma↗

A novel model of senile lung: senescence-accelerated mouse (SAM).

Senescence-accelerated mouse (SAM) has been characterized as a unique animal model to investigate spontaneous aging as well as age-related disorders. However, little is known about the properties of the lung. We examined age-related morphologic and functional changes of the lung in SAM P2, as the senescence-prone strain, and in SAM R1, as the senescence-resistant strain. On morphologic examination, the earlier (starting at 6 mo) and more severe change in airspace size (mean linear intercept: MLI) was observed in SAM P2 (MLI [micron]; 3 mo: 72.1 +/- 2.4; 6 mo: 80.8 +/- 2.9; 12 mo: 91.1 +/- 3.1; 18 mo: 143.4 +/- 6.6), compared with SAM R1 (MLI [micron]; 3 mo: 68.9 +/- 1.8; 6 mo: 70.8 +/- 2.6; 12 mo: 76.1 +/- 2.8; 18 mo: 101.2 +/- 4.7). The destructive index was not remarkably changed through life in both strains, suggesting that the alveolar wall was relatively intact in SAM. On functional examination, the left-sided shift of the pressure-volume (P-V) curves observed in SAM P2 at an early stage of aging (starting at 9 mo) compared with SAM R1. The shape constant (K) obtained from the P-V curve was increased with aging in SAM P2 (K; 3 mo: 0.124 +/- 0.004; 9 mo: 0.142 +/- 0.003; 18 mo: 0.183 +/- 0.008), and also increased at a late stage of aging in SAM R1 (K; 3 mo: 0.123 +/- 0.005; 9 mo: 0.135 +/- 0.004; 18 mo: 0.148 +/- 0.007). This study demonstrates that SAM P2 manifested most of the characteristic changes in senile lung.(ABSTRACT TRUNCATED AT 250 WORDS)

Aging↗

Proteoglycan form of macrophage colony-stimulating factor binds low density lipoprotein.

We recently isolated a proteoglycan form of macrophage colony-stimulating factor (PG-M-CSF) that carries a chondroitin sulfate glycosaminoglycan chain. Here, we examined the interaction of PG-M-CSF with low density lipoprotein (LDL). When LDL preincubated with PG-M-CSF was fractionated by molecular size sieving chromatography, it was eluted earlier than untreated LDL. When LDL was preincubated with chondroitin sulfate-free 85-kD M-CSF instead of PG-M-CSF, the elution profile of LDL remained unchanged, indicating specific interaction between PG-M-CSF and LDL. The level of PG-M-CSF binding in the wells of a plastic microtitration plate precoated with LDL was significant, this binding being completely abolished by pretreatment of PG-M-CSF with chondroitinase AC, which degrades chondroitin sulfate. The addition of exogenous chondroitin sulfate or apolipoprotein B inhibited the binding of PG-M-CSF to LDL in a dose-dependent manner, indicating that the interaction between PG-M-CSF and LDL was mediated by the binding of the chondroitin sulfate chain of PG-M-CSF to LDL apolipoprotein B. PG-M-CSF was also demonstrated in the arterial wall, and there were increased amounts of PG-M-CSF in atherosclerotic lesions. The in vitro interaction between PG-M-CSF and LDL thus appears to have physiological significance.

Aorta↗

Left ventricular function of the heart regressed by nifedipine in spontaneously hypertensive rats.

Left ventricular (LV) performance of the pharmacologically regressed heart in hypertension is still unclear. We compared LV function of the heart regressed by nifedipine with that of the hypertrophied heart in spontaneously hypertensive rats (SHR). Nifedipine (30 mg/kg/day in food) was given to 15-week-old male SHR for 20 weeks (n = 12). Age- and sex-matched SHR served as controls (n = 12). LV catheterization was performed using a micromanometer and cardiac output was determined by the thermodilution method. Hemodynamic studies were performed after washout of nifedipine (24 h), when blood pressure had returned to the untreated level. Peak pumping ability was assessed during acute volume loading with saline. Nifedipine significantly decreased blood pressure in conscious animals (222 +/- 11 to 201 +/- 12 mmHg, p < 0.01) and reduced LV weight (1.20 +/- 0.07 to 1.07 +/- 0.05g, p < 0.01). After washout of nifedipine, LV systolic and end-diastolic pressures, dp/dtmax and cardiac output determined under pentobarbital anesthesia were similar in the treated and untreated groups. Peak pumping ability during acute preload elevation was also similar in the 2 groups. Plasma norepinephrine was unaltered, and plasma renin activity was significantly lower in the treated rats (p < 0.05). These results indicate that nifedipine regressed LVH with a minimal reduction of blood pressure and without evidence of neurohumoral activation or volume retention. In conclusion, LV function of the heart regressed by nifedipine was preserved after a spontaneous rise in blood pressure and during acute preload elevation.

Animals↗

Cloning of the ATP phosphoribosyl transferase gene of Corynebacterium glutamicum and application of the gene to L-histidine production.

Corynebacterium glutamicum mutants lacking ATP phosphoribosyl transferase (PRT) were selected by complementation with the Escherichia coli PRT gene. The recombinant plasmid pCH13 carrying a wild type PRT gene from C. glutamicum T106 was obtained in one of the mutants, LH13. Transformants, LH13/pCH13 and T106/pCH13, had three times higher PRT specific activity than T106. The plasmid pCH99 specifying the PRT, which was desensitized to feedback inhibition by L-histidine fifty-fold higher than the wild type PRT, was derived from pCH13. L-Histidine productivity of C. glutamicum F81, was markedly decreased by pCH13, but increased twice by pCH99. In cultivation in jar fermentors, F81/pCH99 continued to accumulate L-histidine through fermentation and yielded to the titer of 22/5 g/liter, while F81 accumulated only 11.5 g/liter due to production retardation halfway through fermentation. Moreover, F81/pCH99 had a larger production rate than F81 even in its production phase. These results indicate that the yield improvement results from amplification of the highly desensitized PRT provided by pCH99.

ATP Phosphoribosyltransferase↗

Detection of lymphomatous involvement of the lung by bronchoalveolar lavage. Application of immunophenotypic and gene rearrangement analysis.

We report three cases of pulmonary involvement of non-Hodgkin's lymphoma in which immunophenotypic or gene rearrangement analysis of bronchoalveolar lavage (BAL) cells demonstrated monoclonality of T- or B-cell lineage. The first patient had T-cell lymphoma and developed pulmonary lesions. Surface marker analysis of the BAL cells revealed that CD8-positive lymphoid cells were dominant and Southern blot analysis of T-cell receptor gene detected gene rearrangement demonstrating monoclonality of T-cell lineage. The second patient presented with diffuse micronodular shadows on chest radiograph. Marked B-lymphocytosis in BAL fluid prompted us to analyze their clonality. The third was a case in which recurrence of primary pulmonary lymphoma was suspected. In the second and third case, the finding of marked increase in the number of CD 19-positive B lymphocytes with a single class of light chains proved a monoclonal population in BAL cells. With the review of other cases in our study and the relevant literature, we conclude that the clonal analysis of BAL cells is helpful in establishing the diagnosis of pulmonary involvement of T- or B-cell lymphoma.

Adult↗

[Evaluation of mental stress and fatigue induced by performance of a mental task. 2. An experiment in 11-h self-paced calculating task].

An assessment of mental stress and fatigue was undertaken in 12 male students who did their best to perform a calculating task (addition and subtraction of 2-digit numbers) for 11 hours on a workday and rested without any task for 11 hours on a restday. During the work period, occipital midline beta-2 (Oz beta 2) amplitude, urinary adrenaline (A) and noradrenaline (NA) excretion, heart rate (HR), blood pressure (BP), subjective rating of tiredness (SRT), and subjective symptoms of fatigue (SSF) were higher than those during the rest period. Oz beta 2 amplitude, diastolic pressure (DP), critical flicker fusion value (CFF), and performance level (number answered, percent correct) remained unchanged over the rest/work period. Moreover, A and NA excretion, HR, and systolic pressure (SP) changed parallel with their resting level. With the lapse of working hours, SRT and SSF elevated. These results suggest that performance of calculating task causes mental stress which remains constant throughout the work period and that subjective fatigue increases with extension of working hours.

Adult↗

[Diffuse aspiration bronchiolitis (DAB) produced in animals by repeated HCl microaspiration].

We recently reported that diffuse aspiration bronchiolitis (DAB) was detected in 1% of autopsied lungs of aged cases of pneumonia. We hypothesized whether repeated HCl micro-aspiration (RHMA) is involved in DAB and established an animal model by administering HCl intratracheally to rats every two days for 2 weeks. Saline was given to control animals in the same fashion. Then, we performed bronchio-alveolar lavage (BAL) or excised lungs for histologic examination. There was no difference in BAL cell counts, TNF alpha-production, elastase-like activity or albumin levels between the HCl and control groups. Histologically, DAB-like findings were observed in the HCl-treated animals. These data suggest that RHMA might be involved in DAB, while neither TNF alpha-production nor elastase-like activity may play a significant role in inducing DAB.

Animals↗

[A case of pulmonary alveolar proteinosis with elevated serum angiotensin-converting enzyme activity].

A 45-year-old man with diffuse infiltrates on the chest X-ray film was admitted to the hospital. At first, sarcoidosis was suspected due to the elevated serum angiotensin-converting enzyme (ACE) activity. Transbronchial lung biopsy and bronchoalveolar lavage, however, did not lead to that diagnosis. Pulmonary alveolar proteinosis (PAP) was diagnosed after an open lung biopsy. The diffuse infiltrates on his chest X-ray film diminished spontaneously. Two years later, diffuse infiltrates increased again with an elevated serum ACE activity. In this case, it seemed that the severity of PAP was associated with serum ACE activity. We review the literature on the relationship between serum ACE activity and dysfunction of alveolar macrophages in PAP.

Humans↗