[Parenteral hyperalimentation therapy of water-electrolyte imbalance].
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Biomedical subjects
Publications and source records attributed to N Ueda.
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Several naturally occurring prenylflavones were tested for their inhibitory actions on arachidonate 5-lipoxygenase purified from porcine leukocytes. Of the compounds tested, artonin E (5'-hydroxymorusin) exhibited the most potent inhibition on arachidonate 5-lipoxygenase (IC50 = 0.36 microM). Arachidonate 12-lipoxygenase purified from porcine leukocytes and human platelets, 15-lipoxygenase from rabbit reticulocytes and fatty acid cyclooxygenase from bovine vesicular glands were inhibited by the compound only at higher concentrations (IC50 = 2.3, 11, 5.2 and 2.5 microM, respectively).
Three cases of pancreatic tumor in two females (case 1, case 3) and one male (case 2) were reported. Macroscopically cases 1 and 3, which were surrounded by a thick fibrous capsule, developed toward the outside of the pancreas and the cut surface showed mainly cystic degenerative areas filled with necrotic and hemorrhagic materials. In contrast with these two cases, case 2 was buried in the pancreatic tissue and the cut surface showed cystic degenerative areas in its center with a thick fibrous capsule and tumor cell nests invading beyond the capsule to the parenchyma of the pancreas. Microscopically each tumor was identical. The solid areas on the periphery were composed of sheets of polygonal uniform cells subdivided by delicate fibrovascular stalks. Near the degenerative areas, tumor cells lay on a delicate fibrovascular core in one or two layers, with pseudopapillary patterns. Mitotic figures were very rare. All three cases demonstrated immunoreactivity for alpha-1-antitrypsin, but not for islet hormones, tumor markers nor neuron-specific enolase. Although electronmicroscopically, zymogen granules were detected in cases 2 and 3, and annulate lamellae in cases 1 and 3, ductal cell character features were not so developed. From the above, these tumors were diagnosed as solid and cystic tumors of the pancreas. Furthermore, it was suggested that they differentiated in the direction of acinar cells.
The anaesthetic management of a patient with phaeochromocytoma, tricuspid atresia and pulmonary vascular stenosis is reported. The patient received no preoperative preparation with adrenergic blockers. Anaesthesia was induced and maintained with fentanyl, diazepam and sevoflurane. Intraoperative blood pressure was controlled with sodium nitroprusside, sevoflurane, phentolamine, and propranolol. For hypotension after resection of the tumour norepinephrine was required. This patient did not have a systemic to pulmonary shunt procedure performed, so the maintenance of pulmonary blood flow in the presence of haemodynamic instability during operation for phaeochromocytoma was a major concern. Monitoring of oxyhaemoglobin saturation (SpO2) with a pulse oximeter was considered to be useful because SpO2 may reflect pulmonary flow. During serious haemodynamic disturbances due to the manipulation of the tumour, the heart rate was inversely correlated with SpO2, but the relationship between mean arterial pressure and SpO2 was weak. Therefore, control of heart rate appeared to be more important than control of blood pressure in this case.
An HPLC method was based on anion-exchange separation of pyrophosphate (diphosphate) and orthophosphate and postcolumn spectrophotometric detection at 140 degrees C with a molybdenum(V)-molybdenum(VI) reagent. The reagent was easy to prepare, stable for at least 6 months at room temperature, and ready for the determination of pyrophosphate and orthophosphate by the so-called heteropoly blue method without use of any reducing agent. A photodiode-array detector for HPLC indicated the spectral characteristics of the heteropoply blue complex that was detectable at 330-800 nm. The HPLC method had a wide dynamic range from 3 x 10(-7) to 5 x 10(-4) M for both pyrophosphate and orthophosphate with a relative standard deviation of measurement of 10 approximately 2%. Pyrophosphate of 5 x 10(-7) and 5 x 10(-6) M, respectively, could be determined in the presence of a 20,000-fold excess of orthophosphate; 0.01 and 0.1 M.
During bronchoscopy for atelectasis of the middle lobe, a 61-year-old man was found to have a polypoid mass obstructing the bronchus. Right middle and lower lobectomy disclosed a tumor growing into the lumen of the middle lobe bronchus. The histological features of the tumor were indistinguishable from those of the mixed tumor of the salivary gland. A review of the literature reveals only 7 cases of this extremely rare tumor.
5,6,7- and 5,7,8-Trioxygenated 3',4'-dihydroxyflavones were derivatized by introducing alkyl groups of various chain lengths at the 3-position of the flavone skeleton. These compounds were tested as inhibitors for arachidonate 5-lipoxygenase purified from porcine leukocytes. Modification of the 3-position with an alkyl group of 6-10 carbons markedly decreased the IC50 values. 3-Hexyl-3',4'-dihydroxy-5,7, 8-trimethoxyflavone inhibited 5-lipoxygenase with an IC50 value of 58 nM. The platelet and leukocyte 12-lipoxygenases, 15-lipoxygenase of reticulocytes, and cyclooxygenase of vesicular gland were inhibited less potently (IC50 = 0.4, 0.4, 2.7, and 30 microM). Thus, the compound was a relatively selective inhibitor for 5-lipoxygenase.
Several studies indicate an important role of platelet activating factor (PAF) and thromboxane A2 (TXA2) in glomerular pathophysiology. However, the potential role of PAF or TXA2 in renal tubular pathophysiology has received little attention, and the presence of functional receptors for these autacoids in renal tubular epithelium has not been previously studied. We examined the effects of PAF and the TXA2 analogue, ONO11113, on the cytosolic free calcium concentration [( Ca2+]i) in cultured LLC-PK1 cell line using a fluorescent probe, fura-2. In these cells, the addition of PAF or ONO11113 caused a significant increment in [Ca2+]i in a dose-dependent manner: both agonists (10(-7) M) increased [Ca2+]i from 148 +/- 16 to 288 +/- 39 nM and from 130 +/- 8 to 240 +/- 18 nM, with the values of EC50 for PAF and ONO11113 being 17 +/- 4 and 17 +/- 2 nM, respectively. These effects were both rapid and transient, returning to baseline in two minutes. The effect of PAF was selectively blocked by PAF receptor antagonist BN50730, but not by TXA2 receptor antagonist L657925. Similarly ONO11113 response was abolished by L657925, but not by BN50730. PAF- or ONO11113-challenged cells did not respond to a second addition of the same agent and showed heterologous desensitization to the other agonist. The initial peaks of [Ca2+]i as well as the sustained elevations in [Ca2+]i induced by PAF or ONO11113 were reduced following the chelation of extracellular Ca2+ by 10 mM ethylene glycol-bis(beta-aminomethyl ether)-N,N,N',N'-tetraacetic acid (EGTA).(ABSTRACT TRUNCATED AT 250 WORDS)
Cyclosporine A (CSA) stimulated endothelin secretion by a cultured renal epithelial cell line, LLC-PK1. A less nephrotoxic immunosuppressant (FK-506) did not affect endothelin secretion. Putative endothelin converting enzyme inhibitors or specific receptor antagonists may therefore prevent CSA nephrotoxicity.
To determine whether endothelin-1 (ET-1) is released in close proximity to its binding sites on glomerular mesangial cells, and also to elucidate the regulatory factors responsible for its release, we measured immunoreactive ET-1 (ir-ET-1) in the incubation media of isolated glomeruli and cultured mesangial cells of rats using enzyme immunoassay under both basal and thrombin-stimulated conditions. ir-ET-1 was released time-dependently, from isolated glomeruli and cultured mesangial cells. Thrombin (2 U/ml) stimulated the release from both preparations. The release of immunoreactive big endothelin-1 (ir-big ET-1), which was assayed by using enzyme immunoassay, was also time-dependent, and the release was increased by thrombin (2 U/ml; at 4 h, 8 h, and 24 h) in cultured mesangial cells. The releases of big ET-1 and its converted product ET-1 from mesangial cells, an established target for ET-1, suggests that ET-1 acts as an autocrine factor for the cells.
We examined the immunohistochemical distribution of the arachidonate 12- and 15-lipoxygenases in animal and human lung tissue using a polyclonal anti-12/15-lipoxygenase antibody. Immunoblotting of whole cell extracts from bovine and human tracheal epithelial cells or from bovine leukocytes with the antibody (raised originally against purified porcine leukocyte 12-lipoxygenase) showed immunoperoxidase staining of a single protein band (Mr = 72,000), which comigrated with purified bovine 12-lipoxygenase. The antibody also immunoprecipitated both 12- and 15-lipoxygenase activities from cytosolic fractions of bovine and human tracheal epithelial cells. Immunohistochemistry of formaldehyde-fixed and paraffin-embedded bovine (and ovine and canine) trachea using the same polyclonal antibody and an indirect biotin-avidin-peroxidase detection system demonstrated specific staining of tracheal epithelium, polymorphonuclear and mononuclear leukocytes, and perineural cells. Less intense staining of submucosal glands and blood vessels was also observed. Lung sections demonstrated that the level of lipoxygenase antigen decreased markedly by the level of the bronchi and was absent in more distal airways. A similar pattern of immunostaining was found in human lung, except that airway smooth muscle was also weakly reactive, and polymorphonuclear (neutrophilic) leukocytes were unstained (in accordance with the low 12/15-lipoxygenase activity in this cell type). We conclude that animal and human epithelial 12/15-lipoxygenases share enzymatic, antigenic, and regional distribution characteristics and may therefore possess a common function in the pulmonary airway.
Parathyroidectomy is proposed to be protective against gentamicin nephrotoxicity in rats. In the present study, we evaluated the effects of bovine PTH(1-34) on gentamicin accumulation in cultured kidney epithelial cell lines, opossum kidney (OK) cells which possess PTH receptors and LLC-PK1 cells which are devoid of PTH receptors. Ten days after seeding, the culture medium was exchanged for medium containing 1 mM gentamicin and bovine PTH. The cell gentamicin concentration was measured by a substrate-labeled fluorescence immunoassay (TDA gentamicin kit). Gentamicin uptake was accelerated by bovine PTH in OK cells but not in LLC-PK1 cells. The enhancing effect of bovine PTH seems to be mediated by a cAMP-dependent process. The results suggest that PTH accelerates gentamicin accumulation in renal tissues and potentiates gentamicin nephrotoxicity.
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Arachidonate 5-lipoxygenase is an enzyme that catalyzes the oxygenation of arachidonic acid, producing 5-hydroperoxy acid. This enzymatic reaction initiates the biosynthesis of various bioactive leukotrienes. An antiserum was raised in a rabbit against the purified 5-lipoxygenase of porcine leukocytes, and various types of porcine leukocytes were immunostained by use of the antibody. As examined by light and electron microscopy, neutrophils and eosinophils were positively stained. The 5-lipoxygenase was localized in the cytoplasm but not in the plasma membrane and subcellular organelles of the positively stained cells. In contrast, lymphocytes were unstained. In porcine ileum, the majority of 5-lipoxygenase-positive cells were eosinophils and mast cells resident in the lamina propria mucosae, whereas parenchymal cells were not stained. In porcine lung, certain bronchiolar or bronchial epithelial cells were clearly immunostained, in addition to eosinophils and mast cells found in the interstitium.
Twenty-seven previously untreated patients with unresectable non-small cell lung cancer were treated with a 3-drug combination of ifosfamide, cisplatin, and vindesine as a phase II study. Patients received ifosfamide, 1.3g/m2, on days 1 to 5; cisplatin, 20mg/m2, on days 1 to 5; and vindesine, 3mg/m2, on days 1 and 8; with a sufficient parenteral hydration. Courses were repeated every 4 weeks. Twenty males and seven females with a median age of 61 years were treated and fully evaluated. Five patients had stage IIIA, seven had stage IIIB, and 15 had stage IV disease. One patient with adenocarcinoma achieved a complete response and 16 achieved a partial response, for an overall response rate of 63% (95% confidence limit: 45% to 81%). The median duration of response was 34 weeks (range: 9 to 52 weeks). The median survival time was 58 weeks for patients with IIIA/B disease, and 33 weeks for those with IV disease. The major toxicity was myelosuppression, however, it was generally well-tolerated. These results indicate that the 3-drug combination is active against non-small cell lung cancer and warrants further clinical trials.