Release of endogenous adenyl purines from rabbit ear artery.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to K Takeuchi.
Explore the source record for details and available documents.
Several researchers have investigated the relationships between computed tomographic and electroencephalographic abnormalities in schizophrenics. In this present investigation, 28 medicated schizophrenic patients fulfilling the DSM-III-R criteria for schizophrenia and 21 normal volunteers were studied by means of MRI and EEG examinations. All subjects had given informed consent to the investigation. The schizophrenic patients (14 males, 14 females) were aged from 21 to 39 with a mean age of 30.2. The control group consisted of age- and sex-matched healthy volunteers (11 males, 11 females) with no history of neurological disease or head trauma. All the subjects were right-handed as determined by the Edinburgh Inventory. Schizophrenic and control subjects underwent MRI scan and EEG within two weeks. Three trained psychiatrists evaluated patients for BPRS and SANS and the score each item was the median of the three raters. MRI scans were performed by a Asahi Super 200 scanner operating at a 2.0 Tesla magnetic field. A midsagittal scan (8 mm thickness, Spin Echo 500/26) was taken. Subsequently, 15 axial and coronal slices of 5 mm interslice with 2 mm gap were obtained using an Inversion-Recovery sequence (TR: 3000, TI: 800, TE: 14). For measurement purposes, the three MRI scans (Fig-1) were recorded on transparent film, and the boundaries of the cerebral structures were taken traced from the film onto a digitizing tablet. The EEGs were recorded from 16 scalp electrodes of the standard 10/20 system referenced to linked ear electrodes at rest and digitized by a topographic system (Neuromap system MCE-5100, QCE-510B, Nihon Kohden). To calculate EEG power, the frequency spectrum was divided into six EEG frequency bands by 0.25 Hz bands. Each power value was taken from the average percentage of total power and then log-transformed. Schizophrenic patients showed a significantly larger VBR on the axial and coronal planes than control subjects. The areas of the bilateral anterior horns, left body, left posterior horn of the lateral ventricle and the third ventricle were significantly larger in schizophrenic patients than in control subjects. The area of middle half of the corpus callosum in schizophrenic patients was smaller than in control subjects. Schizophrenic patients showed more delta and theta activities in the centro-parieto-occipital regions than control subjects. Schizophrenic patients also showed more beta 1 and beta 2 activities in front-central regions than control subjects. On the other hand, schizophrenic patients showed a markedly decrease in alpha 2 activity in all regions.(ABSTRACT TRUNCATED AT 400 WORDS)
In our department, curative operations were performed for 49 patients with resectable advanced gastric cancer from Jan. 1988 to Feb. 1990. Among these patients, preoperative intra-arterial therapy using cisplatin (40 or 60 mg) was done for 17 patients. In this report, recurrence and survival rate of these patients were investigated. Survival rate of patients with preoperative intra-arterial injection therapy 42 months after operation was 56.15%, while that of patients without preoperative intra-arterial injection therapy was 56.62%. There were no significant differences between these two groups. And two peritoneal disseminations and one brain metastasis were seen in patients with preoperative intra-arterial injection therapy (recurrence rate, 17.6%), but no liver metastasis and local recurrence were noted. Seven recurrences were observed in patients without pre-operative intra-arterial CDDP injection therapy (local 3, liver 3, peritoneal dissemination 1, recurrence rate, 21.2%). We have already reported that much platinum accumulated in gastric cancer tissue and regional lymph nodes. This high accumulation of cisplatin can be the reason why no local recurrence was seen in patients with preoperative intra-arterial injection therapy. In conclusion, preoperative intra-arterial injection therapy using cisplatin may be an effective method to prevent postoperative local recurrence of resectable advanced gastric cancer.
Experimental study of superior mesenteric arterial infusion chemotherapy was done to evaluate the effect of this therapy on metastatic liver tumor. This treatment has been tried clinically for ileus caused by peritoneal carcinomatosis with good result. Moreover, the infused drug is expected to reach the liver via portal route, just like intraportal administration. This study disclosed that superior mesenteric arterial infusion made for a sufficiently high 5-FU concentration of portal blood but the concentration in the metastatic liver tumor was lower when compared with intravenous infusion. However, because the 5-FU concentration in blood of the aorta was lower than in the intravenous administration group, our method may decrease the unfavorable side effects of anti-cancer drugs.
Beta-core fragment (beta-CF), a fragment of the hCG beta-subunit missing its carboxyterminal peptide, can be detected in the urine of women throughout pregnancy or in trophoblastic disease. It is also found in the urine of patients with nontrophoblastic cancers. We examined the beta-CF level in urine samples from patients with cervical cancer and assessed its value as a tumor marker. beta-CF was measured by an enzyme immunoassay with hCG beta-core directed monoclonal antibody No. 229. Based on the cut-off value (0.2ng/ml) from control subjects, the overall positivity rate for urinary beta-CF in the cervical cancer group was 45% (57 of 128 patients), increasing from 32% (23 of 73) in stage I to 100% (2 of 2) in stage IV. These positivity rates exceeded or equaled those of the other markers, SCC, CEA, CA19-9 and CA125, simultaneously measured in the patients' serum. There was no significant difference between the positivity rates for the two histological types of cancer, squamous cell carcinoma and adenocarcinoma. Serial determination in 28 patients with increased urinary beta-CF prior to therapy showed that 24 patients had a decreased concentration after successful treatment, but 2 of 4 patients with still increased urinary beta-CF during or after treatment subsequently relapsed. The determination of urinary beta-CF may provide a useful tool in monitoring the response to treatment in patients with cervical cancer.
In clinical heart-lung transplantation, reperfusion injury is a serious problem. This study was undertaken to evaluate the preventive effect of OP 41483-alpha-CD (OP) as a stable prostaglandin I2 analogue on the reperfusion injury, especially oxygen derived free radicals after the heart-lung transplantation. The heart-lung transplantation was performed according to the Schäefers' method. Explanted heart-lung block was immersed and preserved in the UW solution for just 4 hours at 4 degrees C. In the OP group, OP was administered to the grafts through the pulmonary artery for 25 minutes before and after the reperfusion. No spin adducts were detected in the plasma before harvest of the graft by ESR spectroscopy. But after the onset of reperfusion, free radical in the plasma could be detected. Those signals were 2.007 of the g factor and 15.5 G of the hyperfine splitting constancy (aN). These findings suggested that the free radical detected in the blood of this model was hydroxyl radical. Max dp/dt, left ventricular pressure and cardiac index were higher in the OP group than in the control group after reperfusion, but there was no difference in the left ventricular end-diastolic pressure between two groups. And adenosine triphosphate contents of the myocardial cell was higher in the OP group than in the control group at 60 min after the onset of reperfusion. Oxygenation by the graft's lung was better in the OP group than in the control group after reperfusion. Radical intensities of the plasma by ESR after reperfusion were significantly higher in the pulmonary vein than in the coronary sinus. When OP was administered, radical intensities in the lung and the plasma of the pulmonary vein were significantly lower in the OP group than in the control group. Thiobarbituric acid-reactive substances increased gradually, in two groups with less increase in the OP group. These show that the free radicals, especially.OH generated from the transplanted heart and lung contribute to the reperfusion injury. The platelet counts in the systemic blood, furthermore, did not change appreciably in the OP group, but decreased rapidly in the control group. Probably the microemboli formation was partially inhibited by the administration of OP. Following the onset reperfusion, the free radicals attack the cell membranes and cause the cell damage. When OP was administered through the pulmonary artery, less free radicals were generated in the lung, and the microemboli were possibly inhibited by platelets anti-agglutination. OP administration is useful in the heart-lung transplantation.
In the presence of 1 nM retinoic acid (RA), pentobarbital markedly enhanced differentiation of HL-60 cells to granulocytic cells. In the absence of RA, pentobarbital by itself did not induce cell differentiation. Similarly, pentobarbital enhanced the action of 1,25-dihydroxyvitamin D3 to induce differentiation of HL-60 cells into monocyte/macrophage lineage. The potency of various barbiturates to enhance cell differentiation was closely correlated with their activity to inhibit protein kinase C of HL-60 cells. In contrast to staurosporine, however, barbiturates did not affect the action of differentiation inducers of other types such as dimethyl sulfoxide, dibutyryl cyclic AMP or actinomycin D.
A gene (mdlA) encoding mono- and diacylglycerol lipase (MDGL) from Penicillium camembertii U-150 has been cloned using a 0.9-kb DNA fragment, generated by mixed oligodeoxyribonucleotide (oligo)-primed polymerase chain reaction (PCR), as a probe. Comparison of the nucleotide sequence of the gene and its cDNA clone, obtained by PCR, revealed the presence of two short introns (56 and 53 bp). Two transcription start points (tsp) were localized by primer extension analysis at 37 and 30 bp upstream from the ATG start codon and were preceded by the canonical TATAAA and CAAT sequences. The deduced amino acid (aa) sequence corresponds to 305 aa including a putative signal peptide of 26 aa. Despite significant differences in substrate specificity, the primary structure of the mature region shows homology (29% and 40%) to the triacylglycerol lipases from Mucor miehei and Humicola lanuginosa. Furthermore, the three residues presumed to form the catalytic site, serine, aspartic acid and histidine, are conserved. Primary structure comparisons of MDGL and triacylglycerol lipases are shown.
Acid secretory and mucosal ulcerogenic responses to hypothermia (36-24 degrees C) were examined in anesthetized rats, and the role of thyrotropin-releasing hormone (TRH) in these responses was investigated. Lowering of body temperature (less than 32 degrees C) induced acid hypersecretion and damage in the gastric mucosa. These responses reached a maximum at a body temperature of 28 degrees C and were completely abolished by bilateral cervical vagotomy and significantly inhibited by intracerebroventricular (i.c.v.) administration of TRH antiserum (10 microliters/rat). TRH (10 micrograms/rat) given i.c.v. to the normothermia rat, caused an increase of acid secretion with a pattern similar to those observed during hypothermia. The blood levels of thyroid-stimulating hormone rose significantly during exposure of cold, and this response preceded the onset of acid hypersecretion and lesion formation. Thus, lowering of body temperature induces vagal-dependent gastric acid secretion, probably mediated by TRH released in response to cold exposure, and may be an important element in the etiology of stress ulceration.
A new cobalt-containing nitrile hydratase was purified from extracts of urea-induced cells from Rhodococcus rhodochrous J1 in seven steps. At the last step, the enzyme was crystallized by adding ammonium sulfate. Nitrile hydratase was a 500-530-kDa protein composed of two different subunits (alpha subunit 26 kDa, beta subunit 29 kDa). The enzyme contained approximately 11-12 mol cobalt/mol enzyme. A concentrated solution of highly purified nitrile hydratase exhibited a broad absorption spectrum in the visible range, with an absorption maxima at 410 nm. The enzyme had a wide substrate specificity. Aliphatic saturated or unsaturated nitriles as well as aromatic nitriles, were substrates for the enzyme. The optimum pH of the hydratase was pH 6.5-6.8. The enzyme was more stable than ferric nitrile hydratases. The amino-terminal sequence of each subunit of R. rhodochrous J1 enzyme was determined and compared with that of ferric nitrile hydratases. Prominent similarities were observed with the beta subunit. However, the amino acid sequence of the alpha subunit from R. rhodochrous J1 was quite different from that of the ferric enzymes.
Explore the source record for details and available documents.
The effects of N-ethylmaleimide (NEM), a sulfhydryl (SH) blocker, on ethanol-induced gastric lesions were investigated in rats by varying the route of administration. Oral administration of acidified ethanol (60% ethanol in 150 mM HCl, 1 ml) produced hemorrhagic bandlike lesions in the gastric mucosa. Pretreatment of the animals with orally administered NEM (0.1-10 mg/kg) dose-dependently inhibited these lesions (the inhibition was over 80% at 1 mg/kg or greater), and the effects were partially reversed by indomethacin (5 mg/kg, subcutaneous). However, when NEM (10 mg/kg) was given subcutaneously, this agent significantly worsened the lesions. Intragastrically applied NEM produced a dose-dependent reduction of the transmucosal potential difference (PD) and the mucosal nonprotein SH levels, an increase of the volume of gastric contents, and an inhibition of gastric motility, while these parameters remained unaltered after subcutaneous administration of the agent. The microvascular permeability in the mucosa was significantly increased by both oral and subcutaneous administration of NEM (10 mg/kg) but remained unchanged in response to lower doses of orally administered (less than 3 mg/kg). These results suggest that NEM given orally is cytoprotective to the stomach against ethanol, probably by acting as a mild irritant and due to dilution of an irritant and inhibition of gastric motility (muscle relaxation), but when given subcutaneously it aggravates the lesions by unknown mechanisms.
The pathophysiological changes associated with hypothermia were investigated in the rat stomach under anesthetized conditions. The animal was placed in a styrene foam box and the core body temperature was kept between 24 and 36 degrees C using a heat lamp and refrigerant pack. Lowering of body temperature (less than 30 degrees C) produced acid hypersecretion and induced hemorrhagic lesions in the gastric mucosa; these responses reached the maximum at 28 degrees C, and a significant relationship was found between acid output and lesion score. Hypothermia (28 degrees C) also caused a marked increase of gastric contractile activity and mucosal blood flow (MBF), but the ratio of acid output to MBF became greater when compared to that obtained under normothermic conditions. These changes induced by hypothermia (28 degrees C) were completely blocked by vagotomy and were significantly inhibited by atropine, hexamethonium, clonidine, or TRH antiserum. However, lowering body temperature did not significantly affect acid secretory, motility, and ulcerogenic responses induced by carbachol in the vagotomized rat, excluding local mechanisms (suppression of the inhibitory nerves) in the hypothermia-induced changes. We conclude that hypothermia alone stimulates vagally dependent acid secretion and motility, resulting in damage in the gastric mucosa. These changes may be centrally mediated by TRH, which is released in association with the thermogenic response to hypothermia.
In the present study we have established a pure monolayer culture system of human fallopian tube epithelial cells. The cells were isolated using collagenase digestion, and were cultured in Medium 199 supplemented with 15% fetal bovine serum. The epithelial cells derived from primary and secondary culture were characterized using immunocytochemical staining and electron microscopy. The cells continued to grow for 2 to 3 wk once the monolayer culture of the cells was established. It is currently possible to maintain the cultures until the third generation. Proliferation of these cells was enhanced by epidermal growth factor but not by basic-fibroblast growth factor, insulin, transferrin, estradiol-17 beta, or progesterone. This culture system offers a good model for determining characteristics of the tubal epithelium and would permit effective study of co-culture with embryos.
Plasma levels of platelet-derived growth factor (PDGF) were measured in 24 normal control subjects, 31 patients with stable angina pectoris, 25 patients with unstable angina pectoris, and 31 patients with acute myocardial infarction (AMI) by a sensitive direct radioimmunoassay. The plasma PDGF level in normal control subjects was 273 +/- 25 pg/ml; there was no significant correlation between the plasma PDGF level and age. Plasma PDGF levels in patients with unstable angina pectoris and acute myocardial infarction were significantly lower than those in normal control subjects and patients with stable angina pectoris (p less than 0.05). In patients with acute myocardial infarction the plasma PDGF level in the chronic phase was significantly higher than that in the acute phase (p less than 0.05). These observations raise the possibility that PDGF is involved in the pathophysiology of ischemic heart disease.
The distribution of microtubules and platelet-specific glycoproteins (GPIIb/IIIa) in particles was probed by an immunofluorescence method using anti-tubulin and anti-GPIIb/IIIa antibodies to identify whether particles released from a human megakaryoblastic cell line (MEG-01) are platelets. The fluorescence image showing anti-tubulin staining of the particles revealed a characteristic ring structure observed in platelets. Anti-platelet GPIIb/IIIa antibody staining showed an image in which small patches or spots were seen throughout the particle with brighter staining at the periphery. No significant difference was observed between these particles and human blood platelets under immunofluorescent staining. These results show that MEG-01 cells released platelet-like particles.
The role of capsaicin-sensitive afferent neurons in acid-induced HCO3- secretion was investigated in the duodenum of anesthetized rats. The proximal duodenum was perfused with saline (pH 4.5), the pH of perfusate and the transmucosal potential differences were continuously monitored, and HCO3- output was determined by pH change. Under these conditions, duodenal pH, potential difference, and HCO3- output were significantly increased in response to IV injection of prostaglandin E2 (300 micrograms/kg) and luminal acidification (10 mmol/L HCl, 10 minutes). These responses induced by luminal acid were significantly attenuated by SC pretreatment with indomethacin (5 mg/kg), preexposure of the mucosa to lidocaine (4%, 15 minutes), functional ablation of capsaicin-sensitive afferent neurons, or even prior application of capsaicin (6 mg/mL, 30 minutes) to the duodenum. Although capsaicin application by itself (0.3-6 mg/mL) produced a concentration-dependent increase of HCO3- output, this effect was significantly reduced by lidocaine, indomethacin, or chemical deafferentation and exhibited a tachyphylaxis after repeated application at a high concentration (6 mg/mL). Neither of these treatments significantly affected the HCO3- response induced by prostaglandin E2. It was concluded that stimulation of capsaicin-sensitive afferent neurons increased duodenal HCO3- secretion and that these neurons may be involved in the mechanism of HCO3- response induced by luminal acid in the duodenum.
Circulating immunoreactive endothelin (ir-ET) in the coronary sinus (CS) and the femoral artery (Ao) was measured in patients who underwent percutaneous transluminal coronary angioplasty (PTCA). Plasma ir-ET level in the CS was significantly increased from 1.6 +/- 0.8 pg/mL to 2.0 +/- 1.0 pg/mL after PTCA (P less than .05). Plasma ir-ET level in the Ao tended to increase after PTCA, but it was not significant. Plasma ir-ET level in the CS was not related to the plasma thromboglobulin level, plasma thrombin-antithrombin complex level, mean blood pressure, or heart rate. These results suggest that the increase of plasma ir-ET level in the CS may be associated with the coronary endothelial injury by PTCA.