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  • Electronic Resource  (27)
  • 1995-1999  (20)
  • 1970-1974  (5)
  • 1965-1969  (2)
  • 1
    Electronic Resource
    Electronic Resource
    Oxidation of H-terminated Si(100) surfaces studied by high-resolution electron energy loss spectroscopy (1995)
    [S.l.] : American Institute of Physics (AIP)
    Journal of Applied Physics 77 (1995), S. 5125-5129 
    Details
    ISSN: 1089-7550
    Source: AIP Digital Archive
    Topics: Physics
    Notes: The adsorption of oxygen on H-terminated Si(100) surfaces has been investigated by high-resolution electron energy loss spectroscopy (HREELS). Adsorptions of atomic oxygen occur even at room temperature. Si-OH stretching and Si-O-Si (B1) vibrational modes are observed in HREELS spectra, which indicates that atomic oxygen is adsorbed on sites of Si—H bonds and Si—Si back bonds. On the other hand, H-terminated surfaces are very stable for molecular oxygen, which cannot adsorb until 380 °C on the surface. A dissociative adsorption of molecular oxygen is observed above 380 °C and the activation energy of the adsorption is 2.0 eV at 380–450 °C. This value coincides with the desorption energy of hydrogen atoms from a Si(100) surface with the monohydride phase. These results indicate that the dangling bonds are essential to the adsorption of molecular oxygen on Si(100) surfaces. © 1995 American Institute of Physics.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1063/1.359323
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  • 2
    Electronic Resource
    Electronic Resource
    LACK OF ABNORMALITY IN BRAIN AROMATIC AMINES IN RATS AND MICE SUSCEPTIBLE TO AUDIOGENIC SEIZURE (1969)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 16 (1969), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: The levels of certain amines (catecholamines, 5-HT, and ‘histamine’) and of certain enzymes (tyrosine hydroxylase, tryptophan hydroxylase, ChAc, or AChE) in whole brain or selected brain areas of rats and mice susceptible to audiogenic seizure have been compared with the levels in matched groups of non-sensitive animals. Sensitive groups included both those where susceptibility is inborn and those where it is induced by administration of methionine sulphoximine or thiosemicarbazide. No significant difference was found which could be correlated with susceptibility to audiogenic seizure.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1969.tb08984.x
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  • 3
    Electronic Resource
    Electronic Resource
    Transduction Mechanisms (1968)
    Palo Alto, Calif. : Annual Reviews
    Annual Review of Genetics 2 (1968), S. 245-278 
    Details
    ISSN: 0066-4197
    Source: Annual Reviews Electronic Back Volume Collection 1932-2001ff
    Topics: Biology
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1146/annurev.ge.02.120168.001333
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  • 4
    Electronic Resource
    Electronic Resource
    Role of superoxide anions in airway hyperresponsiveness induced by cigarette smoke in conscious guinea pigs (1996)
    Springer
    Lung 174 (1996), S. 279-289 
    Details
    ISSN: 1432-1750
    Keywords: Guinea pig ; Cigarette smoke ; Airway hyperresponsiveness ; Superoxide
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract To investigate the involvement of superoxide in airway hyperresponsiveness and bronchoconstriction induced by cigarette smoke (CS), we evaluated the effects of superoxide dismutase (SOD), a scavenger of superoxide anion, and apocynin, an inhibitor of superoxide anion-generating NADPH oxidase in phagocytes, on the airway responses induced by CS in conscious guinea pigs. Airway responsiveness was assessed by PC2OOMch, the concentration required to produce a doubling in the baseline specific airway resistance (sRaw) to an inhaled methacholine aerosol, in nonanesthetized spontaneously breathing animals. Before being exposed to ten puffs of CS, animals inhaled either SOD (5,000 units/ml or 25,000 units/ml) or vehicle. Although SOD did not affect PC2OOMch, in the air control group, this agent significantly reduced the CS-induced airway hyperresponsiveness. Repeated administration of apocynin (12 mg/kg for 4 days) did not affect PC2OOMch, after exposure to CS. These data suggest that the superoxide from CS was involved in the airway hyperresponsiveness induced by CS, whereas phagocytic reactive oxygen species were not. The data also suggest a potential therapeutic role for antioxidants in airway hyperresponsiveness.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00176187
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  • 5
    Electronic Resource
    Electronic Resource
    A rat model of HTLV-I infection: development of chronic progressive myeloneuropathy in seropositive WKAH rats and related apoptosis (1995)
    Springer
    Acta neuropathologica 89 (1995), S. 483-490 
    Details
    ISSN: 1432-0533
    Keywords: Key words HTLV-I ; HTLV-I-associated ; myelopathy/tropical spastic paraparesis ; Rat model ; Apoptosis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract In seropositive HTLV-I carrier rats of the WKAH strain inoculated with 2 × 107 MT-2 cells at 3–6 months of age, chronic progressive myeloneuropathy, tentatively designated as HTLV-I-associated myelopathy (HAM) rat disease, occurred when the rats were 19–23 months old. Clinical and pathological findings were basically identical to those of seronegative HAM rats of the same strain neonatally inoculated with MT-2 cells. It appears that a high dose of MT-2 cells (108 cells) is more effective for the induction and acceleration of HAM rat disease. Seronegative and seropositive carriers of other strains (F344, ACI, and LEW), WKAH rats inoculated with HUT-78 (a human T cell line without HTLV-I infection), and untreated WKAH rats at comparable ages did not develop HAM rat disease, thereby indicating that development of this disease is caused by HTLV-I infection and is under strict genetic restriction of the host strain. Chronological examination of HAM rat disease induced by 107 MT-2 inoculation into newborn rats showed that the spinal cord lesion began to develop by 12 months of age. T cells were absent in the affected spinal cord throughout the disease process. There was morphological evidence of apoptotic death of oligodendrocytes in the affected spinal cord. Apoptosis was also confirmed by the specific nick end labeling of the nuclear fragmentation in situ, and the apoptotic oligodendrocytes confined to the demyelinating foci, and the number of apoptotic cells positively correlated with severity of the spinal cord lesion. The collective evidence suggests that the major pathogenetic pathway of HAM rat disease appears to be closely related to apoptotic death of the oligodendrocytes, directly or indirectly associated with HTLV-I infection.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00571502
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  • 6
    Electronic Resource
    Electronic Resource
    A rat model of HTLV-I infection: development of chronic progressive myeloneuropathy in seropositive WKAH rats and related apoptosis (1995)
    Springer
    Acta neuropathologica 89 (1995), S. 483-490 
    Details
    ISSN: 1432-0533
    Keywords: HTLV-I ; HTLV-I-associated ; myelopathy/tropical spastic paraparesis ; Rat model ; Apoptosis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract In seropositive HTLV-I carrier rats of the WKAH strain inoculated with 2×107 MT-2 cells at 3–6 months of age, chronic progressive myeloneuropathy, tentatively designated as HTLV-I-associated myelopathy (HAM) rat disease, occurred when the rats were 19–23 months old. Clinical and pathological findings were basically identical to those of seronegative HAM rats of the same strain neonatally inoculated with MT-2 cells. It appears that a high dose of MT-2 cells (108 cells) is more effective for the induction and acceleration of HAM rat disease. Seronegative and seropositive carriers of other strains (F344, ACI, and LEW), WKAH rats inoculated with HUT-78 (a human T cell line without HTLV-I infection), and untreated WKAH rats at comparable ages did not develop HAM rat disease, thereby indicating that development of this disease is caused by HTLV-I infection and is under strict genetic restriction of the host strain. Chronological examination of HAM rat disease induced by 107 MT-2 inoculation into newborn rats showed that the spinal cord lesion began to develop by 12 months of age. T cells were absent in the affected spinal cord throughout the disease process. There was morphological evidence of apoptotic death of oligodendrocytes in the affected spinal cord. Apoptosis was also confirmed by the specific nick end labeling of the nuclear fragmentation in situ, and the apoptotic oligodendrocytes confined to the demyelinating foci, and the number of apoptotic cells positively correlated with severity of the spinal cord lesion. The collective evidence suggests that the major pathogenetic pathway of HAM rat disease appears to be closely related to apoptotic death of the oligodendrocytes, directly or indirectly associated with HTLV-I infection.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00571502
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  • 7
    Electronic Resource
    Electronic Resource
    Lobar dysmorphism of the kidney: reevaluation of junctional parenchyma using helical CT (1999)
    Springer
    Abdominal imaging 24 (1999), S. 196-199 
    Details
    ISSN: 1432-0509
    Keywords: Key words: Computed tomography (CT), helical—Kidney, CT—Kidney, abnormalities.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract. Background: The term “junctional parenchyma” (JP) has been used to represent many renal anomalies including lobar dysmorphism; however, it has not been evaluated with modalities other than ultrasound (US). Methods: Twenty-two kidneys with lobar dysmorphism incidentally found on helical computed tomography (CT) were studied. In all cases, axial, multiplanar reformation, and three-dimensional images on corticomedullary phase scans were analyzed. Fifteen additional kidneys were prospectively examined with US, and we compared those sonograms with helical CT findings. Results: Comparison of the US and helical CT findings showed that the JP defect and the JP line corresponded anatomically to the upper aspect of the renal sinus and to the thick mural cortex originating from that point, extending inferiorly, respectively. The lesions of lobar dysmorphism were situated deep in the medulla, adjacent to the cortex; however, findings on helical CT did not indicate JP. Conclusions: Although JP may have been seen on US in this study, it did not show fusion remnants of subkidneys but a combination of the upper aspect of the renal sinus, the mural cortex, and the lesion of lobar dysmorphism.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s002619900476
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  • 8
    Electronic Resource
    Electronic Resource
    Hyperresponse in calcium-induced insulin release from electrically permeabilized pancreatic islets of diabetic GK rats and its defective augmentation by glucose (1995)
    Springer
    Diabetologia 38 (1995), S. 772-778 
    Details
    ISSN: 1432-0428
    Keywords: Key words Insulin release ; intracellular calcium ; exocytosis ; GK rat ; permeabilized islets.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary In spontaneously diabetic GK rats, insulin secretion from pancreatic beta cells in response to glucose is selectively impaired, probably due to deficient intracellular metabolism of glucose and impaired closure of KATP channels during glucose stimulation. By using electrically permeabilized islets of GK rats, we explored the functional modulations in exocytotic steps distal to the rise in [Ca2 + ]i in the diabetic condition. At 30 nmol/l Ca2 + (basal conditions) insulin release was similar between GK and non-diabetic control Wistar rats. In response to 3.0 μmol/l Ca2 + (maximum stimulatory conditions), insulin release was significantly augmented in permeabilized GK islets (p 〈 0.01). Raising glucose concentrations from 2.8 to 16.7 mmol/l further augmented insulin release induced by 3.0 μmol/l Ca2 + from permeabilized control islets(p 〈 0.001), but had no effect on that from permeabilized GK islets. The stimulatory effect of glucose on insulin release from permeabilized control islets was partly inhibited by 2,4-dinitrophenol, an inhibitor of mitochondrial oxidative phosphorylation (p 〈 0.01). The hyperresponse to Ca2 + in GK islets may play a physiologically compensatory role on the putative functional impairment both in [Ca2 + ]i rise and energy state in response to glucose in diabetic β cells, and may explain the relative preservation of insulin release induced by non-glucose depolarizing stimuli, such as arginine, from pancreatic islets in non-insulin-dependent diabetes mellitus. [Diabetologia (1995) 38: 772–778]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001250050351
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  • 9
    Electronic Resource
    Electronic Resource
    Pioglitazone time-dependently reduces tumour necrosis factor-α level in muscle and improves metabolic abnormalities in Wistar fatty rats (1998)
    Springer
    Diabetologia 41 (1998), S. 257-264 
    Details
    ISSN: 1432-0428
    Keywords: Keywords Pioglitazone ; muscle TNF-α ; sphingomyelinase ; insulin resistance ; Wistar fatty rat.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary In order to evaluate the relationship between tumour necrosis factor-α (TNF-α) level in muscle and metabolic abnormalities in obesity and diabetes mellitus, pioglitazone, a novel insulin-sensitizing agent, was administered to Wistar fatty rats and time-dependent changes in muscle TNF-α content and plasma indicators of diabetes and obesity were measured. Wistar fatty rats were hyperglycaemic, hyperlipidaemic and hyperinsulinaemic, and their plasma and muscle TNF-α levels were two or more times higher than those in normal lean rats at 16 weeks of age. When pioglitazone was administered to fatty rats at a dose of 3 mg · kg–1· day–1, the plasma triglyceride level and TNF-α levels in plasma and muscle decreased time-dependently, and reached the levels of lean rats within 4 days. Plasma glucose and insulin levels also decreased time-dependently with pioglitazone, but on day 4, these levels were still much higher than the levels in lean rats. Neutral sphingomyelinase (SMase) activity in muscle of fatty rats was two times higher than that in lean rats and was lowered to the level of that in lean rats by 4 days' pioglitazone administration. The plasma leptin level in fatty rats was 8 times higher than that in lean rats, but pioglitazone did not affect the level during the 4-day administration period. These results suggest that an increase in TNF-α production and subsequent activation of SMase in muscle leads to metabolic abnormalities in obesity and diabetes and that antidiabetic activity of pioglitazone is deeply associated with the suppression of TNF-α production. [Diabetologia (1998) 41: 257–264]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001250050901
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  • 10
    Electronic Resource
    Electronic Resource
    Mechanical Properties and Corrosion Resistance of PM High Nitrogen Stainless Steel Consolidated by Hot Extrusion (1999)
    s.l. ; Stafa-Zurich, Switzerland
    Materials science forum Vol. 318-320 (Oct. 1999), p. 681-686 
    Details
    ISSN: 1662-9752
    Source: Scientific.Net: Materials Science & Technology / Trans Tech Publications Archiv 1984-2008
    Topics: Mechanical Engineering, Materials Science, Production Engineering, Mining and Metallurgy, Traffic Engineering, Precision Mechanics
    Type of Medium: Electronic Resource
    URL: http://www.tib-hannover.de/fulltexts/2011/0528/02/04/transtech_doi~10.4028%252Fwww.scientific.net%252FMSF.318-320.681.pdf
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