Gastroesophagostomy after proximal gastrectomy using a double stapling technique.
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Biomedical subjects
Publications and source records attributed to A Sato.
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In experimental models of bronchial asthma with mice, airway inflammation and increase in airway hyperreactivity (AHR) are induced by a combination of systemic sensitization and airway challenge with allergens. In this report, we present another possibility: that systemic antigen-specific sensitization alone can induce AHR before the development of inflammation in the airway. Male BALB/c mice were sensitized with ovalbumin (OVA) by a combination of intraperitoneal injection and aerosol inhalation, and various parameters for airway inflammation and hyperreactivity were sequentially analyzed. Bronchial response measured by a noninvasive method (enhanced pause) and the eosinophil count and interleukin (IL)-5 concentration in bronchoalveolar lavage fluid (BALF) gradually increased following the sensitization, and significant increase was achieved after repeated OVA aerosol inhalation along with development of histologic changes of the airway. In contrast, AHR was already significantly increased by systemic sensitization alone, although airway inflammation hardly developed at that time point. BALF IL-4 concentration and the expression of IL-4 mRNA in the lung reached maximal values after the systemic sensitization, then subsequently decreased. Treatment of mice with anti-IL-4 neutralizing antibody during systemic sensitization significantly suppressed this early increase in AHR. In addition, IL-4 gene-targeted mice did not reveal this early increase in AHR by systemic sensitization. These results suggest that an immune response in the lung in an early stage of sensitization can induce airway hyperreactivity before development of an eosinophilic airway inflammation in BALB/c mice and that IL-4 plays an essential role in this process. If this early increase in AHR does occur in sensitized human infants, it could be another therapeutic target for early prevention of the future onset of asthma.
This study was undertaken to determine whether endothelium-dependent relaxations are altered in mesenteric arteries from young female rats during oestrus cycle and after castration. The contractile response to phenylephrine (Phe) was significantly enhanced in arteries from rats subjected to ovariectomy than in those from sham-operated (control) rats. Treatment of ovariectomized rats with 17beta-oestradiol returned the Phe response to the control level. Arteries from rats at the diestrus stage also exhibited greater contraction in response to Phe. In the presence of 100 microM N(G)-nitro-L-arginine (L-NOARG), the enhancement of the Phe contractile response associated with oestrogen deficiency was not observed. Endothelium-dependent relaxations elicited by acetylcholine (ACh) in arteries precontracted with Phe were significantly reduced in ovariectomized and diestrus rats regardless of whether endothelium-derived nitric oxide (NO) was blocked with L-NOARG. Treatment with 17beta-oestradiol prevented the reduced vascular relaxant response to ACh in ovariectomized rats. The reduction in the ACh responses observed in ovariectomized and diestrus rats was eliminated when 500 nM apamin and 100 nM charybdotoxin were present. ACh-induced endothelium-dependent hyperpolarizations were depressed in arteries from ovariectomized and diestrus rats. The hyperpolarizing response to ACh was significantly improved when ovariectomized rats were treated with 17beta-oestradiol. The resting membrane potentials and pinacidil-induced hyperpolarizations were unaffected by ovariectomy or the diestrus stage. These results suggest that oestrogen-deficient states of both short and long duration reduce the basal release of NO from the endothelium and specifically attenuate endothelium-dependent hyperpolarization and relaxation transduced by endothelium-derived hyperpolarizing factor.
1. 3-Hydroxy-3-methylglutaryl co-enzyme A reductase inhibitors (statins) prevent the progression of atherosclerosis by lowering cholesterol. However, the effect of statins on the synthesis of pro-inflammatory cytokines from endothelial cells has not yet been fully investigated. Here, we examined the effect of pravastatin, one of the statins, on IL-8 synthesis induced by thrombin in human aortic endothelial cells (AoEC) cultured with high glucose concentrations. 2. Pravastatin significantly decreased the IL-8 synthesis induced by thrombin. 3. Pravastatin inhibited the p44/42 MAP kinase activity induced by thrombin, but did not inhibit the p38 MAP kinase activity. 4. Translocation of ras protein from the cytosol to plasma membrane was inhibited by pravastatin. 5. Pravastatin inhibit the activator protein-1 activity, but did not inhibit the activation of IkappaB-alpha. 6. Dominant negative ras inhibited the p44/42 MAP kinase activity induced by PMA. 7. Our results suggest that pravastatin inhibits IL-8 synthesis by blocking the ras-MAP (p44/42) kinase pathway rather than nuclear factor-kappaB. Pravastatin may prevent atherosclerosis not only by lowering cholesterol levels, but also by suppressing IL-8 synthesis in AoEC through the inhibition of p44/42 MAP kinase, and this may be more beneficial in diabetic patients than in non-diabetics.
We present a case of pleurodesis by intrapleural injection of OK-432 for the treatment of fetal chylothorax at an early gestational age. OK-432 injection achieved rapid and effective control of pleural effusion with no adverse effects.
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Dislocation structures and their effect on the superdislocation motion in Ni3Ge single crystals have been studied by two-step deformation. In these tests either octahedral or cube slips were induced by prestraining. A difference in the induced dislocation structure is found to cause a notable change in the second deformation step depending on the combination of the stress axes. In order to understand the orientation sensitive hardening, in-situ deformation experiments have been made on the prestrained specimens in a high voltage electron microscope. Besides observation of the structural change due to dislocation motion, electron irradiation, which decorates antiphase boundary tubes, is utilized to trace the history of the rapid dislocation motion. Based on these observations, the origin of the anomalous strengthening in Ni3Ge is discussed with particular interest in the fine and non-planar dislocation structures induced by cross slips and dislocation-dislocation interactions.
AIMS: To evaluate prolonged QTc interval and QT dispersion as predictors of all-cause and cardiovascular mortality after adjustment for well-established risk factors in Type 1 diabetic patients. METHODS: From a cohort of all adult Type 1 diabetic patients, duration of diabetes >or= 5 years, attending the clinic in 1984 and followed in an observational study for 10 years (n = 939), all subjects with resting baseline electrocardiograms were identified (n = 697, 360 males). The QT length was measured and corrected for heart rate (QTc). Maximal QTc length (QTc max) and QT dispersion were determined. RESULTS: At baseline, 431 had normoalbuminuria (< 30 mg/24 h), 138 had microalbuminuria (30-299 mg/24 h) and 128 had macroalbuminuria (>or= 300 mg/24 h) of whom 66 (15%), 35 (25%) and 61 (48%) died during follow-up, respectively (26 (6%), 14 (10%), 21 (16%) from cardiovascular disease). QTc max. was 442 (1.2) ms (mean (SEM)) for survivors and 457 (3.7) in patients who died (P < 0.001). In a Cox proportional hazards model including baseline values of putative risk factors, independent predictors of death were QTc max (P = 0.03), age (P < 0.001), presence of hypertension (P = 0.001), male sex (P < 0.001), log urinary albumin excretion (P < 0.001), smoking (P = 0.04), log serum-creatinine (P < 0.001), height (P < 0.001), low social class (P = 0.04), whereas QT dispersion, heart rate, and HbA1c were not included. In the subgroup with macroalbuminuria, but not for all patients, QTc max was an independent risk factor for cardiovascular mortality. CONCLUSION: QTc prolongation, but not increased QT dispersion, is an independent marker of increased mortality in patients with Type 1 diabetes mellitus.
The objective of this study was to investigate the state of mupirocin resistance in methicillin-resistant Staphylococcus aureus (MRSA) in a community hospital in Japan. Ninety strains of MRSA were isolated from the respiratory tract of 56 patients (group I, Jun 1990-Aug 1996) before introduction of mupirocin in Japan, which were compared with 168 strains from 48 patients (group II, Sept 1996-Jan 1998) and 146 strains from 85 patients (group III, Feb 1999-Dec 1999) isolated after introduction of mupirocin. Comparisons were made by determining the minimum inhibitory concentrations (MIC) against nine antibiotics. Fifty-five MRSA isolates from 27 patients [13 (27.1%) of 48 in group II and 14 (16.5%) of 85 in group III] after introduction of mupirocin showed low-level resistance to mupirocin (MIC, 6.25 to 50 microg/ml) but the remaining isolates were sensitive to mupirocin (MIC < or =3.13 microg/ml). Most patients colonized with low-level mupirocin-resistant MRSA were elderly (> or =65 years of age), on total parenteral nutrition or nasal feeding and had other underlying diseases. The proportion of patients colonized with low-level mupirocin-resistant MRSA following repeated use of mupirocin was higher in patients of group II than those of group III. Molecular typing by pulsed-field gel electrophoresis (PFGE) demonstrated that the pattern of 13 MRSA isolates from 13 patients of group II consisted of three patterns (A, B, C) with predominance of pattern A, while the pattern of 13 MRSA isolates from 13 patients of group III consisted of three patterns (A, C, D) with predominance of patterns A and D. Our results indicated that resistance of MRSA to mupirocin remains at a low level at present in Japan. However, we should be aware of the possible emergence of MRSA highly resistant to mupirocin in the future.
Familial atrioventricular heart block affected by the autonomic nervous system has rarely been documented. We describe a 35-year-old man who had first-degree atrioventricular heart block with a PR interval of 0.46 s. He had a family history of 2 members with complete heart block and 1 with documented atrial standstill. The man's P-R interval was shortened by exercise and phenylephrine administration. In the electrophysiolgic study, a "split His" with an H-H' of 220 ms was recognized. Such a case of familial atrioventricular heart block with abnormal His-Purkinje conduction affected by the autonomic nervous system is very rare and worthy of description.
The role of environmental compounds with estrogenic activity in the development of male reproductive disorders has been a source of great concern. Among the routes of human exposure to estrogens, we are particularly concerned about cows' milk, which contains considerable amounts of estrogens. The major sources of animal-derived estrogens in the human diet are milk and dairy products, which account for 60-70% of the estrogens consumed. Humans consume milk obtained from heifers in the latter half of pregnancy, when the estrogen levels in cows are markedly elevated. The milk that we now consume may be quite unlike that consumed 100 years ago. Modern genetically-improved dairy cows, such as the Holstein, are usually fed a combination of grass and concentrates (grain/protein mixes and various by-products), allowing them to lactate during the latter half of pregnancy, even at 220 days of gestation. We hypothesize that milk is responsible, at least in part, for some male reproductive disorders.
OBJECTIVE: Our aim was to evaluate the effect of lipopolysaccharide on prostaglandin production and on contraction of isolated myometrial strips from preterm pregnant rats. STUDY DESIGN: Pregnant Wistar rats on day 17 of gestation were killed 3 hours after intraperitoneal injection of lipopolysaccharide (1.5 mg/kg) or vehicle, with or without pretreatment with indomethacin (5 mg/kg administered intraperitoneally) 1 hour beforehand. Concentrations of endotoxin in maternal serum and amniotic fluid, prostaglandin F2alpha and prostaglandin E2 in amniotic fluid, and progesterone in maternal serum were determined. Longitudinal uterine strips were prepared, placed in organ chambers with Krebs-Ringer solution, aerated with 95% oxygen and 5% carbon dioxide (37 degrees C, pH approximately 7.4), and equilibrated at 1g passive tension. Concentration-contraction relationships to oxytocin were determined. Samples of bathing solution were collected 10 minutes after the concentration of oxytocin was maximal. Prostaglandins and progesterone were measured by radioimmunoassay and endotoxin was measured by the Endospecy (Seikagaku Kogyo, Tokyo, Japan) kit. RESULTS: Lipopolysaccharide treatment significantly increased the levels of prostaglandin F2alpha and prostaglandin E2 in amniotic fluid. Treatment with lipopolysaccharide inhibited the production and release of prostaglandin F2alpha and prostaglandin E2 that were activated by oxytocin in uterine strips and increased the sensitivity of strips to the contractile effect of oxytocin. Indomethacin did not affect the basal or the lipopolysaccharide-activated levels of endotoxin in serum and amniotic fluid and exerted a counteraction on lipopolysaccharide-induced increases in concentrations of prostaglandin F2alpha and prostaglandin E2 in amniotic fluid. Indomethacin counteracted oxytocin-activated production and release of prostaglandin F2alpha and prostaglandin E2 in uterine tissues after lipopolysaccharide administration without changing the sensitivity of uterine strips to oxytocin. Concentrations of progesterone were not changed after lipopolysaccharide, indomethacin, or their combined application, which suggests that the changes described were not associated with alterations in the levels of the hormone. CONCLUSIONS: The activation of the uterine contractile system by prostaglandin and oxytocin during intra-amniotic infection may be one of the causes of preterm delivery. A combination of an oxytocin receptor antagonist and an inhibitor of cyclooxygenase may be beneficial in prevention or treatment of preterm labor.
A 32-year-old woman underwent an autologous saphenous vein-covered stent deployment for the treatment of a saccular aneurysm on the distal renal artery. Complete exclusion of the aneurysm was immediately obtained. One year after the treatment, remarkable shrinkage of the aneurysm was demonstrated by means of computed tomography, and wide patency of the renal artery and the stent was shown by means of angiography.
OBJECTIVE: The purpose of this study was to investigate the effects of prolonged (24-h) non-acidemic hypoxemia on plasma endothelin-1 and atrial natriuretic peptide (ANP) in fetal goats. METHODS: During continuous infusion of nitrogen into the maternal trachea, fetal plasma endothelin-1 and ANP levels were measured in nine chronically instrumented goat fetuses at 117-129 days' gestation. Endothelin-1 and ANP were measured by radioimmunoassay. RESULTS: Fetal arterial pO(2) decreased significantly from 23.1 +/- 1.0 mmHg (control) to 15.2 +/- 0.9 mmHg during the first 2 h of hypoxemia and to 15.7 +/- 1.1 mmHg at the end of the experimental period of hypoxemia. The plasma endothelin-1 concentration increased from 10.6 +/- 1.9 pg/ml to 20.4 +/- 4.3 pg/ml (p < 0.05) during the first 2 h and was 19.7 +/- 2.4 pg/ml (p < 0.01) at the end of the experimental period. The plasma ANP concentration also increased, from 20.3 +/- 5.5 pg/ml to 23.0 +/- 4.7 pg/ml in the first 2 h and then to 58.0 +/- 8.8 pg/ml (p < 0.05) at the end of the experimental period. There was a significant negative correlation between fetal plasma endothelin-1 and pO(2), but no significant correlation was found between fetal plasma ANP and pO(2). CONCLUSIONS: Prolonged non-acidemic hypoxemia induces a continuous increase in fetal plasma endothelin-1 and ANP levels. Fetal plasma ANP increases time-dependently but endothelin-1 remains constant during hypoxemia.
Sperm immobilization prior to intracytoplasmic sperm injection (ICSI) is thought to be necessary for efficient fertilization. A variety of methods of sperm immobilization (pipetting, squeezing and piezo application) are currently employed in ICSI. The effect of differences in immobilization method on the timing of initial Ca(2+) oscillations of oocytes in ICSI was investigated. Motile spermatozoa were immobilized in eosin Y solution using pipetting, squeezing and piezo application. Complete staining of the sperm head was achieved after 220.7, 42.2 and 5.0 s respectively. Oscillations after ICSI were measured fluorometrically for each method. The onset of Ca(2+) oscillations was observed at 4.8 to 80.4 min after ICSI. Ca(2+) oscillations developed earlier with the piezo method (14.4 +/- 6.4 min) than other methods (pipetting, 43.1 +/- 20.2 min, P < 0.01; squeezing, 18.4 +/- 3.8 min, P = NS). The piezo method produced the earliest staining of the sperm head and may have caused the most damage to the sperm membrane. A more rapid onset of Ca(2+) oscillations was also observed with the piezo method. The method of sperm immobilization may be important for the rapid release of sperm factors that initiate oocyte activation. This study also showed that Ca(2+) oscillations develop earlier in human oocytes treated by ICSI than indicated in previous reports.
To investigate differences in fertilization mechanisms and the potential clinical use of round/elongated spermatid, we conducted detailed studies of oocyte activation and Ca(2+) oscillation-inducing abilities in these immature sperm cells and compared these abilities against those of mature spermatozoa. When round spermatids from B(6)D(2)F(1) mice were injected, none of the oocytes was activated and no intracellular Ca(2+) ([Ca(2+)](i)) increases were observed. Elongated spermatids could induce activation normally in 87% of injected oocytes, but Ca(2+) oscillation could not be induced at all and most of the oocytes (94%) exhibited only several transient [Ca(2+)](i) rises (transient patterns). Because normal offspring could be obtained when embryos through elongated spermatid injection were transferred to foster mothers, it seems that a normal oscillation pattern of [Ca(2+)](i) is not essential for normal fertilization and embryo development. [Ca(2+)](i) patterns of injected oocytes changed from transient patterns to oscillation patterns while the injected immature sperm cells were maturing to spermatozoa. Dissociations were seen between the timing of appearance of oocyte activation and that of Ca(2+) oscillation-inducing abilities in maturing sperm cells. These dissociations may be due to differences in the thresholds to oocyte activation and Ca(2+) oscillation-inducing factor for inducing oocyte activation and Ca(2+) oscillation.
A series of unnatural base pairs was designed and examined for the expansion of the genetic alphabet and for a better understanding of the mechanism of nucleic acid biosyntheses. To improve the shape complementarity of the previously developed unnatural base pairs, 2-amino-6-(N,N-dimethylamino)purine (x)--pyridon-2-one (y) and 2-amino-6-(2-thienyl)purine (s)--y, the pyrimidine analogue, y, was replaced by a five-member ring, 4-imidazolin-2-one (z), and the s-z pairing in replication was examined. Unnatural bases based on the five-member ring were also applied to the development of non-hydrogen-bonded base pairs.
The 5'-flanking region of the mouse Hex gene was examined in order to identify transcription factors regulating its expression in hepatocytes and haematopoietic cells. We have identified two further GC boxes (GC boxes 3 and 4 at nucleotide positions -149 to -140 and -79 to -70, respectively), i.e. in addition to the two previously determined ones (GC boxes 1 and 2 at nucleotide positions -197 to -188 and -176 to -167, respectively). Luciferase reporter assays revealed that all four GC boxes are transcriptionally active in both MH(1)C(1) rat hepatoma and K562 human chronic myelogenous leukemia cells. Electrophoretic mobility shift assays with specific competitors and antibodies showed that members of the Sp family, namely Sp1 and Sp3, bind to these GC boxes. Overexpression of Sp1 and Sp3 in Drosophila SL2 cells stimulated transcription of the Hex gene through interactions with GC boxes 1 to 4, Sp1 being a more potent activator than Sp3. Thus, we conclude that Sp1 and Sp3 stimulate transcription of the Hex gene in both MH(1)C(1) and K562 cells.