Structural studies of Ga-adsorbed Si(111) sqrt 3-bar x sqrt 3-bar surfaces by low-energy electron diffraction.
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Journal Article↗
Biomedical subjects
K Takeuchi
Publications and source records attributed to K Takeuchi.
Expression of the c-myc gene in human gastrointestinal malignancies.
We have examined the level of the c-myc transcript in 6 esophageal, 16 gastric, 19 colorectal and 1 anal cancer tissue samples; these included four lymph nodes and six hepatic metastases obtained surgically. The esophageal cancer tissues were without an increase of the c-myc transcript, some of the gastric cancer samples showed a two to three fold increase and most of the colorectal and the one anal cancer samples showed a two to ten fold increase when compared with a normal mucosal layer. Therefore, the level of the c-myc transcript in human gastrointestinal malignancies shows organ dependency. Local, lymphatic, and hepatic metastases showed little difference in the level of c-myc mRNA from that of the primary tumor.
Actins↗
An accessory protein identical to mouse egasyn is complexed with rat microsomal beta-glucuronidase and is identical to rat esterase-3.
We report biochemical, immunological, and genetic studies which demonstrate that an accessory protein with the essential features of mouse egasyn is complexed with and stabilizes a portion of beta-glucuronidase in microsomes of rat liver. The accessory protein exists as a complex with beta-glucuronidase since it coprecipitates with beta-glucuronidase after treatment of extracts with a specific beta-glucuronidase antibody. The two proteins are associated by noncovalent bonds since they are easily dissociated at elevated temperatures. Only 20-25% of total liver accessory protein is complexed with microsomal beta-glucuronidase. The remainder exists as a free form. The molecular weight of the accessory protein is 61 to 63 kDa depending upon the rat strain of origin. This protein, like mouse egasyn, has esterase catalytic activity and is concentrated in microsomes. The accessory protein is genetically polymorphic with at least four alleles. Combined biochemical and genetic evidence indicates it is identical with esterase-3 of the rat. Also, both mouse egasyn and rat esterase-3 react with antisera to egasyn and to rat esterase-3, indicating they are homologous proteins. Several inbred rat strains lack microsomal beta-glucuronidase. The same strains lack the accessory protein, suggesting that stabilization of beta-glucuronidase in rat microsomes requires egasyn.
Alleles↗
[Study on histological grading of malignancy of cervical adenocarcinoma].
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Adenocarcinoma↗
Nitrile hydratase of Pseudomonas chlororaphis B23. Purification and characterization.
Nitrile hydratase of Pseudomonas chlororaphis B23 was completely stabilized by the addition of 22 mM n-butyric acid. The enzyme was purified from extracts of methacrylamide-induced cells of P. chlororaphis B23 in eight steps. At the last step, the enzyme was crystallized by adding ammonium sulfate. The crystallized enzyme appeared to be homogeneous from analysis by polyacrylamide gel electrophoresis, analytical ultracentrifuge, and double diffusion in agarose. The enzyme has a molecular mass of about 100 kDa and consists of four subunits identical in molecular mass (approximately 25 kDa). The enzyme contained approximately 4 mol iron/mol enzyme. The concentrated solution of highly purified nitrile hydratase had a pronounced greyish green color and exhibited a broad absorption in visible range with a absorption maxima at 720 nm. A loss of enzyme activity occurred in parallel with the disappearance of the absorption in the visible range under a variety of conditions. The enzyme catalyzed stoichiometrically the hydration of nitrile to amide, and no formation of acid and ammonia were detected. The enzyme was active toward various aliphatic nitriles, particularly, nitriles with 3-6 carbon atoms, e.g. propionitrile, n-butyronitrile, acrylonitrile and cyclopropyl cyanide, served as the most suitable substrates.
Enzyme Stability↗
Role of the prostaglandin-thromboxane system in the development and maintenance of spontaneous hypertension in the rat.
In spontaneously hypertensive rats (SHR) between the ages of 6 and 8 weeks before the development of established hypertension, repeated daily subcutaneous administration of indomethacin, an inhibitor of cyclo-oxygenase, at a dose of 5 mg/kg/day enhanced significantly the development of spontaneous hypertension, but repeated daily subcutaneous administration of OKY 046, an inhibitor of thromboxane (TX)A2 synthetase, at a dose of 12 mg/kg/day did not alter the development of spontaneous hypertension. In SHR between the ages of 15 and 18 weeks with established hypertension, indomethacin or OKY 046 did not alter the high blood pressure as compared with the injection of vehicle. In both young and adult SHR, indomethacin decreased significantly urinary prostaglandin (PG)E2 and TXB2 excretion but not PGE2. These results indicate that cyclo-oxygenase products other than TXA2 may play a protecting role in the development of spontaneous hypertension in the rat whereas their contribution to the maintenance of hypertension may be unlikely. In addition, it is suggested that TXA2 may not be involved in the development and maintenance of spontaneous hypertension in the rat.
Animals↗
Inhibitory effect of sulindac on prostaglandin synthesis in cultured renal and vascular cells.
Sulindac, a non-steroidal anti-inflammatory drug (NSAID), is said to be less toxic to the kidney than the other NSAIDs. To examine this hypothesis we investigated the effects of sulindac and other NSAIDs on prostaglandin (PG) synthesis in cultured rat renal and vascular cells. In all cells examined, indomethacin, tiaprofenic acid, aspirin and ibuprofen (3.3 x 10(-5)-3.3 x 10(-4)M) inhibited both basal and arachidonic acid (AA)-stimulated PGE2 or PGI2 synthesis (measured as 6-keto-PGF1 alpha), while sulindac (3.3 x 10(-5)-3.3 x 10(-4)M) inhibited both basal and AA-stimulated PGE2 synthesis in renal papillary collecting tubule cells but not basal PGI2 synthesis in vascular smooth muscle cells or AA-stimulated PGE2 synthesis in glomerular mesangial cells. The order of potency for NSAIDs to inhibit PG synthesis in these cells was tiaprofenic acid, indomethacin greater than ibuprofen, aspirin greater than sulindac. It is suggested that the prodrug sulindac is biotransformed to the active sulfide in the intact kidney cells, which may be less prominent in glomerular mesangial or vascular smooth muscle cells.
Animals↗
Effect of in vitro aging on prostaglandin synthesis in cultured rat vascular smooth muscle cells.
Cultured rat vascular smooth muscle cells from mesenteric artery produced prostaglandin (PG)E2, PGF2 alpha, PGI2 and thromboxane (TX)A2 in response to arachidonic acid, calcium ionophore A23187, vasopressin and angiotensin II. PGI2 was the major product among these PGs. PG synthesis in these cells decreased with in vitro aging, but the distribution pattern of PG synthesis did not change up to the passage level 56. Therefore, it is suggested that imbalance among PGs may not be directly implicated in vascular diseases in aging.
Aging↗
Irritative and protective activity of mild irritants in rat stomach.
Exposure of the stomach for 30 min to acidified sodium taurocholate (TC) (1-20 mM) or sodium salicylate (SA) (10-80 mM) caused a reduction of transmucosal PD and an increase of luminal pH in anesthetized rats, in a concentration-related manner. Acidified aspirin (ASA) (10-80 mM) reduced PD in the same manner, without significant effect on pH. Histologically, these agents similarly produced damage to the surface cells. After a 30-min exposure to either 20 mM TC or 40 mM SA, acid secretion ceased and bicarbonate (0.5-1 mumol/10 min) appeared in the lumen, whereas acid secretion persisted in the stomach exposed to 40 mM ASA. However, under cimetidine infusion (8 mg/kg/hr) these agents produced similar degrees of luminal alkalinization (approximately 1 mumol/10 min). Pretreatment with indomethacin (5 mg/kg, subcutaneously) significantly inhibited the increase of pH seen after exposure to 20 mM TC, but had no effect on the increase of pH caused by 40 mM SA. Concurrent administration of 16,16-dmPGE2 (3 micrograms/kg, subcutaneously) significantly antagonized the effect of indomethacin in the stomach exposed to 20 mM TC and even increased the pH in the stomach exposed to 40 mM ASA. After a 3-hr exposure to these agents, there was macroscopically apparent damage only in the stomach exposed to ASA, although the PD was similarly reduced in response to either agent. The levels of PGE2 in the corpus mucosa were significantly increased in stomachs exposed to 20 mM TC and 40 mM SA, but decreased in those exposed to 40 mM ASA.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
Role of local motility changes in the pathogenesis of duodenal ulcers induced by cysteamine in rats.
The possible role of local motility in the pathogenesis of duodenal ulcers was investigated in rats using cysteamine. Duodenal motor activity was measured as intraluminal pressure recordings by means of a balloon positioned in the proximal duodenum. Subcutaneous administration of cysteamine (100 mg/kg) produced two linear bandlike lesions in the proximal duodenum within 6 hr. This dose of cysteamine significantly increased gastric acid secretion in acute fistula rats, and decreased duodenal HCO3- secretion caused by acid. During this period, this agent inhibited gastric motility but did produce markedly enhanced contractions in the duodenum. The changes in duodenal motility appeared within 5-10 min and were dose-dependent for cysteamine (10-100 mg/kg). Pretreatment with subcutaneously administered atropine (10 mg/kg), 16,16-dmPGE2 (30 micrograms/kg) or dopamine (10 or 30 mg/kg) significantly reduced the development of duodenal lesions caused by cysteamine, the inhibition being 86.8%, 49.7%, 54.5% or 67.8%, respectively. In the presence of cysteamine, dopamine had minimal effect on both acid and HCO3- secretion, while atropine or 16,16-dmPGE2 markedly inhibited acid secretion or increased HCO3- secretion, respectively. The enhanced duodenal motility induced by cysteamine was blocked partially by atropine and only slightly by 16,16-dmPGE2. Dopamine showed a dose-dependent inhibition on the duodenal hypermotility following cysteamine, and at 30 mg/kg almost completely abolished the development of contractions. These results suggest that abnormal hypermotility in the duodenum may be partly involved in the pathogenesis of cysteamine-induced duodenal ulcers.
16,16-Dimethylprostaglandin E2↗
Evolution of criteria for determination of brain death in Japan.
In 1974, the Japanese EEG Society's Ad Hoc Committee on Brain Death published criteria for determining brain death only in cases of acute gross primary brain lesions. In 1983, a new brain death study group was organized to re-evaluate these criteria. During a 6-month period from March 1, 1984, 217 neurosurgical and neurological clinics and emergency services throughout Japan reported 718 brain deaths caused not only by primary lesions but also by secondary brain lesions and diagnosed as such on the basis of the 1974 criteria excluding the condition of "abrupt fall of blood pressure followed by persistent hypotension". The data derived from the 718 cases in this collaborative study were pooled and analyzed, and it became known that the 1974 criteria still are generally reliable. Some changes have been made, however, and new criteria for determination of brain death adopted.
Advisory Committees↗
Alterations in myocardial systolic and diastolic function in patients with active systemic lupus erythematosus.
Echocardiographic studies were performed to evaluate myocardial function in active patients with systemic lupus erythematosus (SLE). Fourteen patients were studied in the active stage before corticosteroid therapy (active SLE); 10 of them were reexamined after therapy (inactive SLE). Computer-assisted analysis of digitized echoes of the left ventricular dimension was performed. The peak rate of change in dimension during systole (-dD/dt) was reduced in active SLE compared with normal control subjects (2.57 +/- 0.15 cm/sec vs 3.37 +/- 0.14 cm/sec, p less than 0.01). The peak rate of change in dimension during diastole (+dD/dt) was also reduced in active SLE compared with normal control subjects (3.16 +/- 0.19 cm/sec vs 4.41 +/- 0.20 cm/sec, p less than 0.01). After therapy, -dD/dt in inactive SLE was improved compared with active SLE (from 2.56 +/- 0.20 cm/sec to 3.13 +/- 0.19 cm/sec, p less than 0.001). Positive dD/dt in inactive SLE was also improved compared with active SLE (from 3.29 +/- 0.22 cm/sec to 4.23 +/- 0.23 cm/sec, p less than 0.01). No significant differences were found between inactive SLE and normal control subjects as to -dD/dt and +dD/dt. Significant correlations were found between anti-DNA antibody titers and both -dD/dt and +dD/dt (r = -0.97 p less than 0.0001, and r = -0.71 p less than 0.05, respectively). These results suggest that active SLE patients have left ventricular dysfunction that may be caused by an immunopathologic mechanism in SLE.
Adolescent↗
Iatrogenic torsade de pointes induced by thioridazine.
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Adult↗
16,16-Dimethyl prostaglandin E2 aggravates gastric mucosal injury induced by histamine in rats. Possible role of the increased mucosal vascular permeability.
Histamine dihydrochloride (40 or 80 mg/kg, dissolved in 10% gelatin) subcutaneously administered to fasted rats induced few lesions in the gastric mucosa within 4 h. Pretreatment with subcutaneously administered 16,16-dimethyl prostaglandin E2 (dmPGE2; greater than or equal to 10 micrograms/kg) dose-dependently worsened mucosal injury induced by histamine, mostly with severe hemorrhage in the corpus mucosa along the greater curvature, although dmPGE2 alone did not induce any macroscopic damage. The mucosal vascular permeability as measured using Evans blue was slightly but significantly augmented by either dmPGE2 (30 micrograms/kg) or histamine (80 mg/kg) alone, but was markedly increased by histamine in the presence of dmPGE2. The increased vascular permeability occurred within 2 h, and preceded the appearance of hemorrhagic mucosal injury. Both the mucosal injury and the increased vascular permeability caused by histamine (80 mg/kg) in the presence of dmPGE2 (30 micrograms/kg) were significantly reduced by pretreatment with tripelennamine (30 mg/kg) and prednisolone (3 mg/kg), but not affected by atropine sulfate, cimetidine, methysergide, or indomethacin. The stimulation of acid secretion caused by histamine was significantly inhibited by dmPGE2 (30 micrograms/kg). Repeated administration of histamine (40 or 80 mg/kg) in the same area of the stomach in the presence of dmPGE2 (30 micrograms/kg), once or twice daily for 4 days to fed rats, induced more pronounced damage than single-dose treatment. These results suggest that dmPGE2 may aggravate gastric mucosal injury induced by histamine in rats probably due to potentiation of the increased vascular permeability caused by histamine through stimulation of H1-receptors.
Animals↗
Lithium and haloperidol differentially alter the dynorphin A (1-8) and enkephalin levels in the neurointermediate lobe of rat pituitary.
Repeated administration of the antimanic drug lithium (4 mEq/kg/day for 2, 4 or 6 days, i.p.) to rats produced a progressive decline and eventual depletion of dynorphin-A (1-8) (DYN) concentration whereas Met5-enkephalin (ENK) was only marginally decreased in the neurointermediate lobe of the pituitary (NIL). Administration of a neuroleptic haloperidol neither affected ENK and DYN levels nor influenced lithium-induced changes. The study reveals that lithium produces a preferential perturbation in the dynorphin system relative to the enkephalin system. These results taken together with other evidence, indicate that dynorphin is possibly coreleased with vasopressin following lithium administration and provide a pharmacological support to the previously described colocalization and corelease of these endogenous peptides in the NIL.
Animals↗
Lumenal location of the microsomal beta-glucuronidase-egasyn complex.
Mouse liver beta-glucuronidase is stabilized within microsomal vesicles by complexation with the accessory protein egasyn. The location of the beta-glucuronidase-egasyn complex and free egasyn within microsomal vesicles was investigated. Surprisingly, it was found that neither the complex nor free egasyn are intrinsic membrane components. Rather, both are either free within the vesicle lumen or only weakly bound to the inside of the vesicle membrane. This conclusion was derived from release studies using low concentrations of Triton X-100 or controlled sonication. Both the intact complex and free egasyn were released in parallel with lumenal proteins, not with intrinsic membrane components. Also, beta-glucuronidase was protected from digestion by proteinase K by the membrane of microsomal vesicles. The hydrophilic nature of both the complex and free egasyn was confirmed by phase separation experiments with the detergent Triton X-114. Egasyn is one of an unusual group of esterases that, despite being located within the lumen or only weakly bound to the lumenal surface of the endoplasmic reticulum, do not enter the secretory pathway.
Animals↗
In vitro synthesis of influenza viral RNA: characterization of an isolated nuclear system that supports transcription of influenza viral RNA.
An in vitro system for the synthesis of influenza viral RNA was developed using isolated nuclei prepared from influenza virus-infected HeLa cells. In this system, two species of positive-sense RNA, i.e., mRNA and cRNA (complementary RNA to vRNA), were found to be synthesized when analyzed by RNA-RNA hybridization using a minus-strand RNA probe and high resolution gel electrophoresis. The in vitro RNA synthesis required Mg2+, GTP, CTP, UTP, a high concentration of ATP, and an ATP regenerating system. Neither actinomycin D nor alpha-amanitin, potent inhibitors for cellular DNA-dependent RNA polymerases, inhibited the RNA synthesis. Addition of ApG or capped RNA, well-known primers for virion-associated RNA polymerase, markedly enhanced the extent of RNA synthesis. The maximum activity was observed with nuclei isolated from cells at 5 h after infection. This system is useful for the purification and characterization of factors involved in the transcription of these two species positive-sense RNA.
Adenosine Triphosphate↗
Renal kallikrein activity in spontaneously hypertensive rats.
To assess possible roles of the renal kallikrein-kinin system in the development of spontaneous hypertension, we determined daily excretion of urinary total and active kallikrein in 6-week-old spontaneously hypertensive rats (SHR) and Wistar-Kyoto (WKY) rats for up to 2 weeks. We also evaluated the effect of aprotinin, a reversible inhibitor of kallikrein and other serine proteases, on the development of hypertension in the 6-week-old SHR on ordinary intakes of sodium or on sodium loading with 1% NaCl for up to 2 weeks. Active kallikrein was determined by its kininogenase activity, and the generated kinins were radio-immunologically measured. Total kallikrein was also determined by measuring kininogenase activity after inactive kallikrein had been activated with trypsin (200 micrograms/ml). Urinary active kallikrein excretion was significantly reduced in 7-week-old SHR (1.5 +/- 0.2 microgram/day compared to 2.8 +/- 0.3 micrograms/day in WKY, P less than 0.05) and in 8-week-old SHR (1.6 +/- 0.2 microgram/day compared to 3.2 +/- 0.4 micrograms/day in WKY, P less than 0.01). Urinary total kallikrein excretion was also reduced in the 7- and 8-week-old SHR whereas the ratio of active to total kallikrein did not change. In addition, renal contents of total and active kallikrein were significantly lower in the 8-week-old SHR than in the controls.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗