Metabolic effects of carteolol and dilevalol in essential hypertension.
Explore the source record for details and available documents.
Carteolol↗
Biomedical subjects
T Baba
Publications and source records attributed to T Baba.
Immunocytochemical study of dystrophin in cultured mouse muscle cells by the quick-freezing and deep-etching method.
Dystrophin, the protein product of the Duchenne muscular dystrophy (DMD) gene, is deficient in patients with DMD and in mdx mice. It is immunocytochemically localized in skeletal muscle sarcolemma. However, little is known about the three-dimensional ultrastructural localization of dystrophin and its relationship with other cytoskeletal proteins. We found that dystrophin is localized irregularly, just underneath the plasma membrane in normal cultured mouse myotubes, by using the quick-freezing and deep-etching (QF-DE) method; it was found to be closely linked to actin-like filaments (8-10 nm in diameter), most of which were decorated with myosin subfragment 1, and was attached to the cytoplasmic side of the plasma membrane. These results suggest that dystrophin might play an important role in the preservation of cell membrane stability by connecting actin cytoskeletons with the cytoplasmic side of the plasma membrane.
Animals↗
Immunohistochemical study of skin lesions in herpes zoster.
Thirty-seven biopsy skin tissues of herpes zoster taken from 27 patients were analysed immunohistochemically using two monoclonal antibodies detecting either nucleocapsid or glycoproteins of varicella-zoster virus (VZV) on paraffin sections of formalin fixed tissues. Skin lesions of herpes zoster were divided clinically into four stages: erythematous, vesicular, pustular and ulcerative. In the erythematous stage, VZV antigens, if detected, were found only within ballooning cells in the lower epidermis or follicular epithelium. In the vesicular stage, antigens were detected in the cells around and within the intraepidermal vesicles and in histiocytes or fibrocytes of the dermis in all cases and in the endothelial or perineural cells in 10 of 14 cases. In the pustular stage, the antigens were observed in degenerated or necrotic keratinocytes and multinucleated giant cells within pustules and some necrotic cells in the dermis. In the ulcerative stage, the viral antigens were detected only at the ulcer margin and around the hair shaft in 2 of 7 cases. These results suggest that VZV initially involves the epidermis in the erythematous stage, subsequently invades the dermis in the vesicular stage, and disappears in the early ulcerative stage.
Antigens, Viral↗
Acute effect of an alpha 1-adrenoceptor antagonist on urinary sodium excretion, plasma atrial natriuretic peptide, arginine vasopressin, and the renin-aldosterone system in healthy subjects.
To elucidate the mechanism underlying the sodium retention caused by alpha 1-adrenoceptor blockade in man, a placebo-controlled, randomised, double-blind study has been made of the acute effects of bunazosin an alpha 1-antagonist, on urinary sodium excretion, atrial natriuretic peptide (ANP), arginine vasopressin (AVP), and the renin-aldosterone system in 7 healthy men. A single oral dose of bunazosin 2.0 mg caused a significant reduction (P less than 0.05) in urinary sodium excretion after 0-2 h, 2-4 h, and 4-6 h. The mean values for plasma ANP, AVP, aldosterone, and cortisol concentrations at those times were similar after placebo and bunazosin, and plasma renin activity was significantly increased 2 and 4 h after bunazosin. Pretreatment with oral enalapril 10 mg, an angiotensin converting enzyme inhibitor, did not prevent the bunazosin-induced reduction in urinary sodium excretion. There was a significant positive correlation between the drug-induced changes in blood pressure and urinary sodium excretion. The results suggest that ANP, AVP, and renin-aldosterone may play little role in the sodium retention caused by acute alpha 1-adrenoceptor blockade in man.
Adrenergic alpha-Antagonists↗
Three-dimensional study of epithelioid cells by a quick-freezing and deep-etching method in muramyl dipeptide-induced granulomas.
The three-dimensional ultrastructure of epithelioid cells was studied by the quick-freezing and deep-etching (QF-DE), as well as the freeze-substitution (QF-FS) methods. The granulomas were induced in rats by injecting muramyl dipeptide (MDP) into the hind footpads. At 3 weeks after the injection, the footpads were perfused with a fixative, excised, and quickly frozen to prepare the replica membranes. Some unfixed footpads were also quickly frozen and freeze-substituted. Dense networks of intermediate filaments, connected with the nuclei, mitochondria and other vesicular cell organelles, were observed throughout the cytoplasm of epithelioid cells by the QF-DE method. A few actin filaments were located in filopodia and just beneath the cell membranes. Interdigitation of the cell membranes between adjacent cells was clearly demonstrated by the QF-FS method and clathrin-coated pits were identified at the base of interdigitating filopodia. In addition, the exact moment of fusion between endosomes and lysosomes was ascertained by the same method. These results suggest that the cytoskeletal organization of epithelioid cells resembles that of epithelial cells rather than actively motile macrophages.
Acetylmuramyl-Alanyl-Isoglutamine↗
Properties of the enzyme expressed by the Pseudomonas saccharophila maltotetraohydrolase gene (mta) in Escherichia coli.
The maltotetraohydrolase gene (mta) from Pseudomonas saccharophila was expressed in Escherichia coli JM109. Maltotetraohydrolase was produced mostly (approximately 90%) in the periplasmic space. The amino-terminal amino acid sequence and molecular weight of the recombinant enzyme were identical with those of the native enzyme, and there was no significant difference in the substrate specificity and modes of action. This system for maltotetraohydrolase expression is useful for studies of the structure and function of the enzyme.
Blotting, Western↗
Effects of theophylline on the selective increases in intratumoral blood flow induced by intracarotid infusion of adenosine and adenosine triphosphate in C6 glioma-transplanted rat brains.
We have previously reported that the intracarotid administration of adenosine or adenosine triphosphate (ATP) selectively increased blood flow in intracerebrally transplanted C6 glioma cells in rats, using the hydrogen clearance method. In the present paper, we studied the difference between the effects of adenosine and ATP, using theophylline, a P1 purinoceptor blocker. The selective enhancement of the tumor blood flow by intracarotid administration of adenosine was almost totally inhibited by theophylline. In contrast, the selective enhancement by ATP was shown definitely not to be inhibited by theophylline. Therefore, it is supposed that the selective increase of intratumoral blood flow by the intracarotid infusion of adenosine is closely related to the P1 purinoceptor, and the effect of the intracarotid infusion of ATP is composed not only of the effect as degraded into adenosine but also of the effect of ATP itself.
Adenosine↗
Glycaemic control and progression of nephropathy in proteinuric NIDDM patients.
Explore the source record for details and available documents.
Biomarkers↗
Starch branching enzymes from immature rice seeds.
Four forms of branching enzyme, termed RBE1, RBE2 (a mixture of RBE2A and RBE2B), RBE3, and RBE4, were apparently separated by DEAE-cellulose column chromatography of soluble extract from immature rice seeds, and each of these four forms was further purified by gel-filtration. RBE1, RBE2A, and RBE2B were the predominant forms of the enzyme. The molecular size, amino-terminal amino acid sequence, and immunoreactivity with anti-maize branching enzyme-I (BE-I) antibody were identical among these three forms, except that the molecular mass of RBE2A was almost 3 kDa higher than those of RBE1 and RBE2B. These results indicate that RBE1, RBE2A, and RBE2B are the same (termed rice BE-I). The cDNA clones coding for rice BE-I have been identified from a rice seed library in lambda gt11, using the maize BE-I cDNA as a probe. The nucleotide sequence indicates that rice BE-I is initially synthesized as an 820-residue precursor protein, including a putative 64- or 66-residue transit peptide at the amino terminus. The rice mature BE-I contains 756 (or 754) amino acids with a calculated molecular mass of 86,734 (or 86,502) Da, and shares a high degree of sequence identity (86%) with the maize protein. The consensus sequences of the four regions that form the catalytic sites of amylolytic enzymes are conserved in the central region of the rice BE-I sequence. Thus, rice BE-I as well as the maize protein belongs to a family of amylolytic enzymes.
1,4-alpha-Glucan Branching Enzyme↗
The effects of interferon-beta on phorbol ester or calcium ionophore-induced intercellular adhesion molecule-I expression in epidermal carcinoma cells.
Keratinocyte intercellular adhesion molecule (ICAM)-I expression is induced by interferon (IFN)-gamma. It has been previously reported that IFN-beta suppresses IFN-gamma-induced ICAM-I expression in A431 cells, a human squamous cell carcinoma cell line. In this study, the suppression mechanisms were investigated at the post second messenger level. Both 12-O-tetradecanoylphorbol-13-acetate (TPA) and calcium ionophore (A23187) induce ICAM-I expression in A431 cells. ICAM-I expression induced by either was not suppressed with cotreatment with IFN-beta. Furthermore, IFN-beta did not inhibit the translocation of protein kinase C (PKC) by TPA. It appears that the pathways involved in ICAM-I expression induced by activation of PKC or increased in intracellular Ca++ are not affected by IFN-beta.
Calcimycin↗
SecY variants that interfere with Escherichia coli protein export in the presence of normal secY.
As an approach for studying how SecY, an integral membrane protein translocation factor of Escherichia coli, interacts with other protein molecules, we isolated a dominant negative mutation, secY-d1, of the gene carried on a plasmid. The mutant plasmid severely inhibited export of maltose-binding protein and less severely of OmpA, when introduced into sec+ cells. It inhibited growth of secY and secE mutant cells, but not of secA and secD mutant cells or wild-type cells. The mutation deletes three amino acids that should be located at the interface of cytoplasmic domain 5 and transmembrane segment 9. We also found that some SecY-PhoA fusion proteins that lacked carboxy-terminal portions of SecY but retain a region from periplasmic domain 3 to transmembrane segment 7 were inhibitory to protein export. We suggest that these SecY variants are severely defective in catalytic function of SecY, which requires cytoplasmic domain 5 and its carboxy-terminal side, but retain the ability to associate with other molecules of the protein export machinery, which requires the central portion of SecY; they probably exert the 'dominant negative' effects by competing with normal SecY for the formation of active Sec complex. These observations should provide a basis for further genetic analysis of the Sec protein complex in the membrane.
Alkaline Phosphatase↗
Antigen presentation by Toxoplasma-infected cells: antigen entry through cell membrane fusion.
The antigen presentation of cells infected by Toxoplasma gondii (T.g.) for MHC class-I-restricted cytotoxic T cells (CTL) was blocked by treating the T.g.-infected cells with the fungal antibiotic brefeldin A. Electron microscopic analysis of T.g.-infected murine and human-antigen-presenting cells (APC) prepared by the combination of quick-freezing with the deep-etching or freeze-substitution methods revealed that the outer membrane of T.g. fused with some parts of the vacuolar membranes of APC to build up channel-like structures. Work station and cytofluorometry studies detected 2',7'-bis(carboxyethyl)-5(6)-carboxyfluorescein (BCECF) in cells infected by BCECF-labeled T.g., which strongly suggested the direct entry into cells of BCECF derived from T.g. These findings provide evidence that T.g. antigens enter the cytoplasm of APC through cell membrane fusion of T.g. and T.g.-infected APC, and that T.g.-infected APC present T.g. antigen for MHC class-I-restricted CTL through the endogenous pathway of antigen presentation.
Animals↗
Microsurgical and magnetic resonance imaging anatomy of the cerebello-medullary fissure and its application during fourth ventricle surgery.
The cerebellomedullary fissure, the only entrance or exit to the fourth ventricle, is surrounded rostrally by the cerebellar tonsils and the biventral lobules and caudally by the medulla oblongata, the tela choroidea, and the lateral recesses. This fissure is an important route in operations on the fourth ventricle. We studied the microsurgical and magnetic resonance imaging (MRI) anatomy of the fissure by using autopsied normal cerebellum. MRI revealed that the fissure is visible as a slit and is indicated by the enhanced choroid plexus and the flocculus. Oriented by the anatomical information thus obtained, we have surgically treated nine patients with a tumor either in or around the fourth ventricle. Preoperative MRI clearly demonstrated the tumors in relation to the cerebellomedullary fissure. It revealed the precise anatomical location and extension of the tumor, not only its inferior extension but also its lateral one. The MRI findings and microsurgical anatomy of the cerebellomedullary fissure were quite useful for the removal of the tumors in the fourth ventricle.
Aged↗
Inflammatory cell infiltrates vary in experimental primary and metastatic brain tumors.
We have studied the cellular immune response that accompanies primary and metastatic brain cancers induced experimentally in rats by inoculation of RG-2 glioma and Walker 256 (W256) carcinoma cells, respectively. The inflammatory cell infiltrates were characterized with lectin histochemistry to visualize microglial cells and macrophages and with immunohistochemistry, using a panel of monoclonal antibodies, to detect major histocompatibility complex (MHC), lymphocytic, and macrophage antigens. The metastatic tumor was composed of a loose stroma with multiple, often large, necrotic areas, whereas the RG-2 glioma was composed of a dense collection of tumor cells showing only rare necrotic foci. Both tumor types were heavily infiltrated with microglia and/or macrophages, and these were positive for MHC Class II (Ia) antigens. Expression of MHC Class I antigens was absent from RG-2 glioma cells, but it was present in W256 metastatic carcinoma cells. The metastatic tumor was also characterized by a much heavier infiltrate of lymphocytes, as shown by the presence of cells positive for CD4, CD8, and leukocyte common antigens. These lymphocytic markers were absent from reactive microglia in the W256 carcinoma, whereas they were present in the RG-2 glioma. Polymorphonuclear leukocytes were seen only in the metastatic tumor. Our study delineates differences between the inflammatory cell infiltrates found in metastatic brain tumors and those found in primary brain tumors. The differences in cell composition and immunophenotype may indicate a more effective antitumor response in the metastatic tumor that could account for the observed tissue destruction.
Animals↗
Normal blood pressure in patients with insulinoma despite hyperinsulinemia and insulin resistance.
This article examines the relationship between blood pressure and serum insulin patients with endogenous hyperinsulinemia due to insulinomas. The hypothesis that hyperinsulinemia is an independent causal factor in the development of essential hypertension in this patient population was investigated. Inappropriately high plasma concentrations of insulin and proinsulin were found in these patients; however, their blood pressure levels did not differ from those of normal control subjects. Moreover, the surgical removal of the insulinomas did not reduce their blood pressure. Therefore, these findings argue against the hypothesis that hyperinsulinemia is an independent causal factor in the development of essential hypertension in humans.
Blood Pressure↗
Recent advances in pharmacological management of hypertension in diabetic patients with nephropathy. Effects of antihypertensive drugs on kidney function and insulin sensitivity.
Hypertension is often seen in Type 1 and Type 2 diabetic patients, particularly in those with nephropathy, and the progression of diabetic nephropathy is closely related to blood pressure elevation. Thus, the effects of antihypertensive drugs on kidney function and insulin sensitivity in diabetic patients are of great clinical importance. Successful antihypertensive treatment has been shown to slow the progression of diabetic nephropathy. Several results from short term studies have suggested that angiotensin converting enzyme (ACE) inhibitors may be advantageous over other conventional antihypertensive agents in reducing albuminuria in both hypertensive and normotensive diabetics with microalbuminuria or persistent proteinuria. However, the decline in glomerular filtration rate during ACE inhibitor treatment is comparable to that during effective treatment with conventional antihypertensive drugs in hypertensive Type 1 diabetic patients with overt nephropathy. Whether ACE inhibitors possess a specific effect in preventing the development of diabetic nephropathy remains to be seen in properly designed long term studies. Although calcium antagonists may preserve kidney function or possess a renoprotective effect in hypertensive Type 2 diabetics with nephropathy, firm evidence supporting this contention seems to be lacking and also requires long term evaluation. Increasing attention is being directed toward the effect of antihypertensive drugs on insulin sensitivity in diabetic patients: ACE inhibitors and alpha 1-adrenoceptor blocking agents have been shown to improve this sensitivity. Despite the widespread involvement of calcium in hormone secretion and action, calcium antagonists appear to have little effects on the glucoregulatory and calcium-regulatory hormones within the drug dosages used in clinical practice. Several clinical variables, such as the presence or absence of hypertension, overt nephropathy and microalbuminuria, or a combination of variables should be accounted for when evaluating critically the cumulative data on the effects of antihypertensive drugs on kidney function and albuminuria in the variety of diabetic patient groups. Understanding the pharmacokinetic and pharmacodynamic characteristics of antihypertensive drugs will be of clinical importance in diabetic patients with advanced nephropathy (glomerular filtration rate of less than 30 ml/min) and/or other complications, such as impaired gastric motility or gastroparesis, and will thereby lead to a more rational management of hypertension in those patients.
Antihypertensive Agents↗
The effect of 5-lipoxygenase inhibition on blood-brain barrier permeability in experimental brain tumors.
To determine if leukotrienes are important mediators of vascular permeability in brain tumors, the effect of 5-lipoxygenase inhibitors on blood-tumor barrier permeability in rats harboring HK Walker 256 brain tumors was examined using quantitative autoradiography with alpha-14C-aminoisobutyric acid. The 5-lipoxygenase enzyme converts arachidonic acid to leukotrienes. Three 5-lipoxygenase inhibitors were utilized: BW755C, nordihydroguaiaretic acid, and AA-861. All three 5-lipoxygenase inhibitors significantly decreased vascular permeability both within the tumors and in brain adjacent to tumor. This suggests that capillary permeability in and adjacent to tumors is influenced by endogenous leukotrienes and that leukotrienes play an important role in brain tumor edema.
4,5-Dihydro-1-(3-(trifluoromethyl)phenyl)-1H-pyraz↗
Selective blood-tumor barrier disruption by leukotrienes.
The authors have previously reported that intracarotid infusion of 5 micrograms leukotriene C4 (LTC4) selectively increases blood-tumor barrier permeability in rat RG-2 tumors. In this study, rats harboring RG-2 tumors were given 15-minute intracarotid infusions of LTC4 at concentrations ranging from 0.5 microgram to 50.0 micrograms (seven rats in each dose group). Blood-tumor and blood-brain barrier permeability were determined by quantitative autoradiography using 14C aminoisobutyric acid. The transfer constant for permeability (Ki) within the tumors was increased twofold by LTC4 doses of 2.5, 5.0, and 50.0 micrograms compared to vehicle alone (90.00 +/- 21.14, 92.68 +/- 15.04, and 80.17 +/- 16.15 vs. 39.37 +/- 6.45 microliters/gm/min, respectively; mean +/- standard deviation; p less than 0.01). No significant change in Ki within the tumors was observed at the 0.5-microgram LTC4 dose. Blood-brain barrier permeability was selectively increased within the tumors. At no dose in this study did leukotrienes increase permeability within normal brain. To determine the duration of increased opening of the blood-tumor barrier by LTC4 administration, Ki was measured at 15, 30, and 60 minutes after termination of a 15-minute LTC4 infusion (seven rats at each time point). The mean Ki value was still high at 15 minutes (92.68 +/- 15.04 microliters/gm/min), but declined at 30 minutes (56.58 +/- 12.50 microliters/gm/min) and 60 minutes (55.40 +/- 8.10 microliters/gm/min) after the end of LTC4 infusion. Sulfidopeptide leukotrienes LTC4, LTD4, LTE4 and LTF4 were infused to compare their potency in opening the blood-tumor barrier. The mean leukotriene E4 was the most potent, increasing the permeability value 3 1/2-fold compared with vehicle alone (139.86 +/- 23.95 vs. 39.37 +/- 6.45 microliters/gm/min).
Analysis of Variance↗