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Biomedical subjects

M Iwata

Publications and source records attributed to M Iwata.

At least 325 records · Page 18Linked to original sources

Molecular basis for subtypic differences of the "a" subunit of coagulation factor XIII with description of the genesis of the subtypes.

The "a" subunit of human coagulation factor XIII (F13A) exhibits genetic polymorphism defined by four common alleles, F13A*1A, *1B, *2A, and *2B. We have previously suggested on the basis of the isoelectric focusing patterns of the four allele products that point mutations at two separate sites and one intragenic crossing over might be involved in the genes of F13A polymorphism. Here, we report nucleotide substitutions associated with F13A polymorphism. A C/T transition of the second nucleotide of codon 564 in exon 12 is responsible for the difference between F13A*1A and *1B and that between F13A*2A and *2B, and a set of two base changes in codons 650 and 651 in exon 14 leads to the differences between F13A*1A and *2A and those between F13A*1B and *2B. The four combinations of the point mutations at the two exons thus correspond to the four alleles, two of which were generated by the point mutations from ancestral monomorphic gene. The results suggest strongly that intragenic crossing over must be involved in the genesis of the fourth allele. Polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) methods discriminating these base changes in exons 12 and 14 are also presented.

Alleles↗

Gonadotropin releasing hormone (GnRH) neurons project to growth hormone and somatolactin cells in the steelhead trout.

Analysis of gene expression using gonadotropin-releasing hormone (GnRH) antisense oligonucleotide confirmed by immunocytochemical localization the occurrence of GnRH neurons along the nervus terminalis in the steelhead trout (Oncorhynchus mykiss). Double-label immunocytochemistry revealed the distribution of mammalian (m), salmon (s) and chicken II (cII)-type GnRHs and various pituitary hormones. Both sGnRH and mGnRH appeared to be colocalized in the same cells of the nervus terminalis. Chicken GnRH II-immunoreactivity was found only in fibers and terminals. In the younger fish [73 and 186 days after fertilization (DAF)] GnRH neurons were seen rostral to the olfactory bulb. A novel GnRH ganglion, along the nervus terminalis, was found at the cribiform bone (gCB). A few non-immunoreactive rounded cells were seen among the GnRH neurons. A second smaller ganglion was seen at the most rostrally located part of the ventromedial olfactory bulb (gROB). In the older fish (850 DAF) GnRH neurons were also observed in the basal forebrain. A small group of neurons (2-3 cells), at the caudoventromedial border of the olfactory bulb, formed the ganglion terminale. Occasionally isolated GnRH-immunoreactive cells were seen at the base of the olfactory epithelium, along the ventromedial margins of the olfactory nerve. GnRH-immunoreactive and GnRH mRNA expressing neurons were absent from midbrain regions at the ages observed. GnRH-immunoreactive fibers were present only in older fish. The pattern of distribution of fibers that were immunoreactive to all three forms of GnRH was identical. Fibers were seen along the medial side of the olfactory nerve, throughout the brain and in the pituitary, associated with growth hormone and somatolactin cells.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Surgical treatment of hepatocellular carcinoma.

The effect of surgical treatment for hepatocellular carcinoma (HCC) was evaluated in 149 resected cases, 83.2% of which were associated with liver cirrhosis. The 3- and 5-year survival rates were 60.1% and 39.4%, respectively. The mortality rate was 4.1%. In patients aged over 70 years, liver cirrhosis was found in 53.3% of cases and the mortality rate was 6.7%. The 3- and 5-year survival rates were 50.8% and 33.9%, respectively. Factors that significantly affected survival for more than 5 years were a tumor size of less than 3 cm, Stage I disease, vp(-), IMo, and diploid type. The 5-year survival rate for patients with a single tumor of 3 cm or less was 54.2%, regardless of the surgical procedure. All 15 patients with a solitary tumor of 2 cm or less (Stage I, small liver tumor) were alive with a 5-year survival rate of 100%. The problem is the treatment of patients with a tumor measuring 3-5 cm in diameter and associated liver cirrhosis, because their prognosis after surgery is the worst. HrS (subsegmentectomy) is the minimal procedure of limited hepatectomy for these cases with postoperative multidisciplinary therapy.

Adult↗

Pathophysiology of dogs after 84% hepatectomy with emphasis on prostaglandin metabolites and the effect of a thromboxane A2 synthesis inhibitor and a prostaglandin I2 analog.

The pathophysiological conditions following 84% hepatectomy were examined in terms of the changes in thromboxane A2 (TxA2) and prostaglandin I2 (PGI2) in a canine model. OKY-046, a TxA2 inhibitor, and OP-2507, a PGI2 analog, were administered to evaluate the possibility of extending hepatic resection. The 2-week survival rate following 84% hepatectomy significantly improved after the administration of OKY-046 and OP-2507, from 12.5% to 58.3% and 75.0%, respectively. Furthermore, OP-2507 significantly improved impaired hepatocyte and sinusoidal endothelial cell function after 84% hepatectomy, resulting in a satisfactory recovery to the preoperative levels. Within 24 h after 84% hepatectomy, the plasma levels of thromboxane B2 (TxB2) increased significantly, and the 6-keto-prostaglandin F1 alpha (6-KF) levels became slightly elevated. OKY-046 and OP-2507 decreased TxB2 and increased 6-KF in the plasma, resulting in the maintenance of sufficient blood flow in the portal vein and hepatic tissue and the mitigation of microcirculatory disorders. Moreover, the cytoprotective effects of the two drugs inhibited functional impairment of the residual liver. In conclusion, abnormal prostaglandin metabolites were produced after 84% hepatectomy, being involved in residual liver disorders. However, the administration of either an inhibitor of TxA2 synthesis or a PGI2 analog ameliorated the functional impairment of the residual liver, which suggests their potential value for extending the resectability of the liver from what is presently feasible.

6-Ketoprostaglandin F1 alpha↗

Diffuse panbronchiolitis: diagnosis and distinction from various pulmonary diseases with centrilobular interstitial foam cell accumulations.

Diffuse panbronchiolitis (DPB) is a clinicopathologic entity characterized histologically by chronic inflammation principally affecting the respiratory bronchioles. Few pathologists outside Japan are familiar with this entity. The most distinctive pathologic feature of DPB is chronic inflammation and an accumulation of foam cells in the walls of the respiratory bronchioles, adjacent alveolar ducts, and alveoli (PB unit lesion). The differential diagnosis is important both clinically and histologically because of the similarity of DPB to other chronic airway diseases. We report seven cases of DPB and 20 examples of a histologically similar lesion (PB-like lesion) found in a large review of cases of bronchiolitis, cystic fibrosis, bronchiectasis, aspiration pneumonia, extrinsic allergic alveolitis. Wegener's granulomatosis, bronchocentric granulomatosis, and malignant lymphoma. The results indicate that the PB-like lesion is a nonspecific histologic finding; the diagnosis of DPB can be made only in the appropriate clinical setting and when other conditions have been carefully ruled out.

Adult↗

Calcium accumulation following middle cerebral artery occlusion in stroke-prone spontaneously hypertensive rats.

Delayed neuronal damage in the ischemic region of the rat brain following middle cerebral artery (MCA) occlusion in stroke-prone spontaneously hypertensive rats was studied. The distribution of neuronal damage was determined by 45Ca autoradiography. Accumulation of 45Ca was observed in the corpus callosum and ipsilateral cerebral cortex immediately following MCA occlusion. After 3 days of occlusion, 45Ca had accumulated in the ipsilateral pyramidal tract, the ventral posterior nucleus of the thalamus, and the lateral portion of the striatum. Significant accumulation of 45Ca was observed in the same areas after 7 and 14 days of occlusion. Next the effect of MK-801 on accumulation of 45Ca after MCA occlusion was examined using the same technique. MK-801 (0.5-10 mg/kg i.v.) or saline was administered 15 min before MCA occlusion, and volumes of accumulation of 45Ca were calculated 1 week after ischemic insults. MK-801 significantly reduced 45Ca uptake in the cortex, striatum, and thalamus. Furthermore, there was a strong statistical correlation between the volume of accumulation of 45Ca in the cortex and that in the thalamus (r = 0.8974; p < 0.001; n = 25). We speculate that delayed neuronal damage in the corpus callosum, ipsilateral pyramidal tract, and thalamus may be caused by secondary neuronal degeneration. However, neuronal damage in the striatum, a segment not supplied by the MCA, may be related to excessive release of glutamate.

Animals↗

Post-ischemic acute renal failure protects proximal tubules from O2 deprivation injury, possibly by inducing uremia.

Rats within the early maintenance phase of post-ischemic acute renal failure (ARF) can resist additional ischemic insults. This study assessed whether this protection exists directly at the tubular cell level, and if so, whether it is a consequence of prior cell injury (for example, due to heat-shock protein synthesis; HSP), or if it arises in response to reductions in functional renal mass and/or the uremic environment. Rats were subjected to either 15 or 35 minutes of unilateral or bilateral renal ischemia, and after 15 minutes to 24 hours of reflow, proximal tubular segments (PTS) were isolated for study. Their viability following oxygenation and hypoxic/reoxygenation injury (H/R) was tested (LDH release). The influence of uremia/reduced renal mass was determined by studying PTS extracted 24 hours after 1 1/2 nephrectomy, and by determining whether PTS exposure to a "uremic milieu" (urine addition) blocks H/R damage. HSP effects were gauged by correlating renal cortical HSP-70 expression with degrees of in vitro protection, and by ascertaining whether in vivo hyperthermia (42 degrees C; 15 min) mitigates subsequent PTS H/R damage. Results were compared with those obtained from normal PTS. The in vivo experimental protocols did not substantially alter PTS isolation or their viability during oxygenation. Fifteen minutes of ischemia induced neither azotemia nor PTS cytoprotection. In contrast, 35 minutes of ischemia conferred marked protection against subsequent H/R, but only when azotemia was permitted to develop (protection seen after 24 hr, but not at 4 hr of reflow; protection abrogated by retention of 1 normal kidney). Renal failure in the absence of tubular necrosis (1 1/2 uninephrectomy) protected PTS from H/R damage.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Kidney Injury↗

Involvement of protein kinase C-epsilon in glucocorticoid-induced apoptosis in thymocytes.

Apoptosis is induced in immature thymocytes by physiological peak levels of glucocorticoid hormones, especially in murine and rat cells. Endogenous glucocorticoids may have some role in thymic selection. Glucocorticoid-induced thymocyte apoptosis appears to be dependent on protein kinase C (PKC), since it is inhibited by PKC inhibitors. PKC is a family of closely related enzymes, consisting of Ca(2+)-dependent (PKC-alpha, -beta I, -beta II, and -gamma) and Ca(2+)-independent (PKC-delta, -epsilon, -eta (L), -theta, -zeta, and -lambda) isozymes. In the present study, we analyzed the role of PKC in glucocorticoid-induced apoptosis in murine thymocytes and found that glucocorticoid selectively induces an increase in Ca(2+)-independent PKC activity in the particulate fraction of immature thymocytes but not in that of mature T cells. The increase as well as the apoptosis was inhibited by actinomycin D, cycloheximide, or the glucocorticoid receptor antagonist, RU 38486. Immunoblotting studies revealed the selective translocation of PKC-epsilon from the cytosolic fraction to the particulate fraction upon glucocorticoid treatment. These results suggest that glucocorticoid-induced apoptosis in immature thymocytes involves glucocorticoid receptor-mediated and selective activation of PKC-epsilon through de novo synthesis of macromolecules.

Animals↗

Naming difficulties in alexia with agraphia for kanji after a left posterior inferior temporal lesion.

The case is described of a patient with alexia and agraphia for kanji, and severe anomia after a subcortical haemorrhage in the left posterior inferior temporal area. Magnetic resonance imaging at four months after onset showed a lesion in the inferior temporal and fusiform gyri, extending from the temporo-occipital junction toward the anterior third of the temporal lobe. Comparison with other reported cases of alexia with agraphia and anomia made it clear that when accompanied by severe anomia, the lesions extended either forward to the anterior part of the middle temporal gyrus or medially to the parahippocampal gyrus. It is suggested that the disconnection of association fibres between the parahippocampal, fusiform, middle, and inferior temporal gyri, especially between the parahippocampal gyrus and the other temporal gyri, or the cortical damage to the posterior part of these gyri is essential for the production of anomia.

Aged↗

Differences in the effects of two hexachlorobiphenyls on superoxide generation by polymorphonuclear leucocytes stimulated by N-formyl-methionyl-leucyl-phenylalanine and phorbol myristate acetate.

The effects of hexachlorobiphenyls (HCBs) on superoxide (O2-) generation by guinea pig polymorphonuclear leucocytes were examined. 2,3,6,2',3',6'-HCB by itself had only a weak inductive effect on O2- generation. This compound, however, enhanced O2- generation stimulated by N-formyl-methionyl-leucyl-phenylalanine (FMLP) about twofold, but not the generation induced by phorbol myristate acetate (PMA). On the other hand, 3,4,5,3',4',5'-HCB suppressed O2- generation stimulated by both FMLP and PMA. The inhibitory potency of this compound was far greater with PMA (ID50, 5 microM) than with FMLP (ID50, 40 microM).

Animals↗

An evaluation of renal tubular DNA laddering in response to oxygen deprivation and oxidant injury.

It has recently been suggested that endonuclease activation and/or apoptosis, possibly triggered by oxidant stress, are important pathogenetic mechanisms in oxygen deprivation/reoxygenation-induced proximal tubular cell death. To explore this possibility, DNA "laddering," a characteristic feature of these processes, was sought in: (1) postischemic rat kidneys (25- or 40-min arterial clamping; 0, 1, 4, 8, 24, and 48 h and 6 days reflow); (2) posthypoxic isolate rat proximal tubular segments and (3) cultured human kidney proximal tubular cells (HK-2) subjected either to energy depletion plus Ca2+ overload (antimycin A plus 2-deoxyglucose plus Ca2+ ionophore A23187), or to H2O2-induced cell death. DNA was subsequently extracted, electrophoresed through agarose gels, and visualized with ethidium bromide or Southern blotting. To maximize ladder detection, DNA samples were also end-labeled with 32P dideoxyadenosine triphosphate with terminal deoxynucleotidyl transferase (tdt), followed by electrophoresis. None of the postischemic DNA samples demonstrated any laddering by either ethidium bromide staining or Southern analysis (apoptotic lymphocyte DNA was a positive control). However, trace laddering was apparent by the tat technique, commencing at 1 h of reflow, peaking at 24 h, and resolving slowly thereafter. This finding correlated with the morphologic expression of tubular necrosis, not apoptosis. Hypoxia/reoxygenation caused proximal tubular segment death (44 to 64%), and HK-2 cells were slowly killed by both the H2O2 and the energy depletion/Ca(2+)-loading protocols. However, neither protocol induced ethidium bromide- or tdt-detectable DNA laddering. It was concluded that: (1) minimal DNA laddering develops postischemia, and this change is reliably detected only by the tdt method; (2) it correlates with the morphologic expression of tubular necrosis, not apoptosis; and (3) in vitro oxidative- and energy depletion-mediated proximal tubular cell death can be dissociated from DNA ladder formation.

Animals↗

[Study on the aging influence on the recognizability for colored targets--black and color].

Recently spaces for the aged have become more wide spread as the population of them has increased. Most of the spaces, however, are originally provided for the young and, accordingly, can not be considered preferable environments for the aged. From this point of view, the authors aimed at the visual environments for the aged and carried out experimental research on the influences that aging gives to recognizability for colored targets, for the purpose of providing a preferable visual environment for the aged. The results show that the recognizability for colored targets declines drastically from about fifty years old, as just as the recognizability for uncolored targets. Moreover, the results show that, although the recognizability of the young is considerably influenced by differences of the illuminance and color of the target surfaces, aging made the recognizability less influencable by these differences.

Adolescent↗

Dyskeratosis congenita showing usual interstitial pneumonia.

A 46-year-old man was admitted to our hospital with cough and dyspnea on exertion. A chest X-ray film showed diffuse interstitial shadows. He had hyperpigmentation forming a network pattern around his neck and dystrophy of the fingernails and toenails, and was diagnosed as having dyskeratosis congenita. Histological examination of the lung specimen obtained from the left S4b by open lung biopsy revealed usual interstitial pneumonia pattern with neither asbestos bodies nor silicotic nodules. Taken together with previously published findings, pulmonary involvement is considered to be an important complication of dyskeratosis congenita.

Age Factors↗

The role of kinins and atrial natriuretic peptide on the renal effects of neutral endopeptidase inhibitor in rats.

To further elucidate the natriuretic mechanisms of neutral endopeptidase 24.11 (NEP) inhibition, we employed a new specific NEP inhibitor, UK 73967 (UK), with or without a specific kinin receptor antagonist, Hoe 140 (Hoe), in Sprague-Dawley rats, and evaluated the renal NEP, kinins and plasma ANP simultaneously. There were no significant changes in urinary NEP, kinins, urine volume (UV) or urinary sodium excretion (UNaV) with vehicle treatment in anesthetized normotensive rats. Infused UK (10 mg/kg) significantly decreased NEP, and increased kinins, UV and UNaV. There was not a significant difference in plasma ANP between the vehicle and UK groups. Simultaneous administration of Hoe (20 nmol/kg) canceled the increases of UV and UNaV caused by UK. From these results, we conclude that inhibition of NEP may exaggerate the contribution of renal kinins to the renal water-sodium metabolism and overcome the contribution of ANP on that metabolism at least in normotensive rats.

Animals↗

Growth stimulator for bifidobacteria produced by Propionibacterium freudenreichii and several intestinal bacteria.

A bifidogenic growth stimulator was present in the cell-free filtrate of Propionibacterium freudenreichii 7025 culture and in the methanol extract fraction of the cells. Several intestinal bacteria, such as Bacteroides, Enterobacter, and Enterococcus, which also released a growth stimulator for bifidobacteria, may play an important role in regulation of a bifidobacterial population in colonic microflora. The water-soluble stimulator from the methanol extract of the cells was partially purified. The molecular weight of the stimulator appeared to be < 3000. The stimulatory activity was unaffected by treatments with pronase, carboxypeptidase A, ribonuclease, or nuclease P1 and was heat stable over a wide pH range. This stimulator differed from cyanocobalamin and from organic acids, such as acetate and propionate. Because it was stable to heat and proteolytic enzymes, the stimulator is a useful bifidogenic factor that can reach the large intestine while retaining its activity. Short-chain fatty acids were highly inhibitory to the growth of many intestinal bacteria, particularly Gram-negative facultative and obligatory anaerobes. The short-chain fatty acids (especially propionate) stimulated the growth of bifidobacteria. The growth of Bifidobacterium adolescentis 6003 was further enhanced in the presence of short-chain fatty acids and the stimulator produced by P. freudenreichii 7025. Viable counts of strain 6003 grown with Bacteroides vulgatus JCM 5826T increased more than 10(4) over those of the single culture of strain 6003. However, the growth of strain 6003 was inhibited in the mixed culture with Clostridium perfringens 7028. In continuous culture, the growth of bifidobacterial strain 6003 could be greatly enhanced, even in the presence of clostridial strain 7028, in media with short-chain fatty acids and stimulator produced by P. freudenreichii 7025.

Bacteroides↗

[A case of sarcoidosis associated with severe cardiac conduction disturbances and unilateral pleural effusion].

A 23-year-old man was admitted to our hospital because of non-productive cough. Chest X-ray demonstrated bilateral hilar lymphadenopathy, bilateral infiltration shadows and right pleural effusion. ECG showed complete A-V block and sinus arrest. Transbronchial lung biopsy and pleural biopsy specimens showed non-necrotizing epithelioid cell granulomas. The patient was diagnosed as having sarcoidosis, and was treated with steroid and pacemaker. After steroid therapy, myocardial imaging with thallium-201 showed increase of uptake and the pleural effusion disappeared.

Adult↗

[A case of respiratory bronchiolitis-associated interstitial lung disease].

We report the first case of respiratory bronchiolitis-associated interstitial lung disease in Japan. A 48-year-old man with a 36-pack-year smoking history was referred because of 6 months of dry cough. Chest X-ray showed bilateral reticulonodular shadows. HRCT scan showed bilateral reticulonodular and ground glass shadows with centrilobular distribution. BAL yielded 85 x 10(6) cells with 99.5% macrophages. Histologic examination of the biopsy specimen obtained under thoracoscopy showed evidence of respiratory bronchiolitis, with accumulation of pigmented macrophages within respiratory bronchioles and adjacent air spaces associated with mild thickening of the peribronchiolar interstitium.

Bronchiolitis↗