Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:Q9UID3 (FFR)
 233 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Basic LM, TEM, SEM, and FFR appearances of a pure line of normal human melanocytes derived from foreskin, and a human melanoma line, in cell culture are described. Normal melanocyte cultures exhibit side by side, cells of widely different melanogenic activities--possible clones--and melanosomes of bizarre shape and internal structure are frequent. Aggregates of melanosomes, with or without associated amorphous material, and with no discernible limiting membrane are present within many cells, and occasional simple specialised contacts occur between apposed cells. On replicas of plasma membrane of normal melanocytes, particle densities and diameters on P and E fracture faces were within the ranges for cells in general, and equivalent data for the melanoma cells were not significantly different. Similarly, there was no difference in density of distribution or diameter of nuclear pores between the normal and the tumoural cells.
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PMID:Transmission and scanning electron microscopy and freeze-fracture replication of normal human melanocytes and human melanoma cells in tissue culture. 323 99

We investigated whether glycolysis was necessary to maintain the integrity of vascular endothelial and alveolar epithelial barriers in continually weighed isolated rabbit lungs. Lungs were perfused with a cell-free buffered salt solution, and glycolysis was inhibited with a glucose analogue (alpha-methyl glucoside, alpha-MG) or one of two glycolysis inhibitors (iodoacetic acid, IAA, or NaF). Fluid filtration rates (FFR's, the change in lung weight/time) in response to a 7.5-min zone 3 hydrostatic stress (pulmonary arterial and venous pressures raised from 8 to 15 cmH2O, alveolar pressure kept constant at 4 cm on the deflation limb) were repeatedly measured for 120 min after which the lungs were lavaged. The total protein concentration was measured in the bronchoalveolar lavage fluid (BALP). Lactate production was measured to verify inhibition of glycolysis. Lower concentrations of IAA and alpha-MG eliminated lactate production but did not affect FFR or BALP. NaF also had no effect on the FFR or BALP. Only high concentrations of IAA increased FFR and BALP, seemingly by causing nonspecific membrane injury that was unrelated to its specific effects on glycolysis. The glycolytic pathway for energy production is not necessary to maintain the integrity of the pulmonary endothelial-epithelial barrier.
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PMID:Glycolysis is not required for fluid homeostasis in isolated rabbit lungs. 340 35

Two auditory neurophonic responses - one recorded from the scalp (frequency following response or FFR) and one from the auditory nerve (auditory nerve neurophonic or ANN) - were obtained following stimulation of the cat cochlea with amplitude-modulated (AM) high-frequency tones. The carrier frequencies varied between 2 and 30 kHz. The modulation frequencies varied between 400 and 3000 Hz. The AM responses were compared with pure-tone neurophonic responses. The AM response waveforms were found to have a similar spectral composition, similar rates of adaptation, and similar rates of recovery from forward masking as the comparable pure-tone responses. As with the pure-tone neurophonics, an unmodulated masking stimulus can produce prolonged depression of the probe response. The amount and duration of this depression is dependent upon the level and frequency of the masker. The frequency dependence of the depression is demonstrated by forward masked tuning curves which indicate that the AM responses arise from fiber populations which have restricted characteristic frequency distributions centered on the carrier frequency. Response amplitude as a function of stimulus level (I/O) functions, response amplitude as a function of carrier frequency (carrier transfer functions or CTF) and response amplitude as a function of modulation frequency (modulation transfer functions or MTF) were also measured. It was found that the I/O functions were saturating monotonic functions of stimulus intensity, CTFs were flat for carrier frequencies from 6 to 30 kHz, and MTFs were flat for modulation frequencies from 100 to 1500 Hz. These results are compared with similar data for single units and compound action potentials.
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PMID:Auditory neurophonic responses to amplitude-modulated tones: transfer functions and forward masking. 342 51

A major problem in spinal cord injury research is quantification of motor function in animals. Most investigators in the field currently use neurologic scoring systems, relying on subjective observations of complex behaviours and assigning scores based on arbitrary criteria. These scoring scales are prone to observer bias and are nonspecific. We describe here a simple, reproducible, noninvasive, and objective test of a limited aspect of spinal motor function in cats, based on a well-known involuntary response of animals to sudden free fall. Free fall responses, or FFRs, have been studied in many species, including man, and are thought to be carried in ventral and lateral column pathways, i.e., vestibulospinal, reticulospinal, and rubrospinal tracts. We recorded the FFRs from hind and forelimb muscles of 100 cats before and after thoracic spinal cord injury. Hindlimb FFRs were shown to have three quantifiable components: a fast synchronous activation (E1) followed by a short silent period during which spinal segmental reflexes are inhibited (I1) and a late desynchronized excitatory burst (E2). Thoracic spinal injury produced hindlimb FFR losses ranging from greatly reduced amplitude to complete absence of response. Residual FFRs correlated with the extent of ventral column preservation and locomotory ability. Individual FFR components can be preserved. For example, some injured cats exhibited only 11 responses. Our work suggests that FFRs are a reliable and sensitive test of motor recovery in spinal cord injury.
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PMID:The vestibulospinal free fall response: a test of descending function in spinal-injured cats. 633 48

The contribution of the catalytic and noncatalytic domains of factor IXa to the interaction with its cofactor, factor VIIIa, was evaluated. Two proteolytic fragments of factor IXa, lacking some or all of the serine protease domain, failed to mimic the ability of factor IXa to enhance the reconstitution of factor VIIIa from isolated A1/A3-C1-C2 dimer and A2 subunit. Both fragments, however, inhibited this factor IXa-dependent activity. Selective thermal denaturation of the factor IXa serine protease domain eliminated its effect on factor VIIIa reconstitution. Modification of factor IXa with dansyl-Glu-Gly-Arg chloromethyl ketone (DEGR-IXa) stabilized this domain, and heat-treated DEGR-IXa retained its ability to enhance factor VIIIa reconstitution. These results indicate the importance of the serine protease domain as well as structures residing in the factor IXa light chain (gamma-carboxyglutamic acid and/or epidermal growth factor domains) for cofactor stabilizing activity. In the presence of phospholipid, the A1/A3-C1-C2 dimer produced a saturable increase in the fluorescence anisotropy of fluorescein-Phe-Phe-Arg chloromethyl ketone-modified factor IXa (Fl-FFR-IXa). This effect was inhibited by a factor IXa fragment comprised of the gamma-carboxyglutamic acid and epidermal growth factor domains. The difference in Fl-FFR-IXa anisotropy in the presence of A1/A3-C1-C2 dimer (delta r = 0.043) compared with factor VIIIa (delta r = 0.069) represented the contribution of the A2 subunit, A peptide corresponding to factor VIII A2 domain residues 558-565 decreased the factor VIIIa dependent-anisotropy of Fl-FFR-IXa to a value similar to that observed with the A1/A3-C1-C2 dimer. These results support a model of multiple interactive sites in the association of the enzyme-cofactor complex and localize sites for the A1/A3-C1-C2 dimer and the A2 subunit to the factor IXa light chain and serine protease domain, respectively.
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PMID:Localization of factor IXa and factor VIIIa interactive sites. 759 60

This study was designed to investigate the effects of angiotensin II (AII) receptor antagonist and angiotensin converting enzyme (ACE) inhibitor on insulin resistance, and the mechanism by which ACE inhibitor improves insulin-dependent glucose uptake (insulin sensitivity) in an insulin-resistant hypertensive rat model (fructose-fed rats, FFR) and in essential hypertensives (EHT). Male Sprague-Dawley rats were fed on fructose-rich or standard chow for 4 weeks and treated either with 10 mg/kg/day of delapril (n = 8), 1 mg/kg/day of TCV-116 (AII receptor antagonist; n = 13), or vehicle (n = 9) for the latter 2 weeks. Steady-state plasma glucose (SSPG) was measured with the subjects in the conscious state; simultaneously, we infused insulin (2.5 mU/kg/min) and glucose (8 mg/kg/min) to determine insulin sensitivity in each group. Thirteen EHT were hospitalized and the 2-h euglycemic hyperinsulinemic glucose clamp (GC) method was performed in a fasting condition before and after 2 weeks' administration of TCV-116 (8 mg/day) in 7 EHT and of delapril (120 mg/day) in 6 EHT. Insulin sensitivity was evaluated as M-value calculated from the infusion rate of glucose. Mean blood pressure (MBP) was higher in FFR (137.7 +/- 73.8 mm Hg, P < .05) compared to controls (120.8 +/- 2.7 mm Hg), and was lower in both the delapril (108.1 +/- 6.3 mm Hg, P < .05) and TCV-116 (112.8 +/- 4.3 mm Hg, P < .05) groups than in FFR.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of angiotensin receptor antagonist and angiotensin converting enzyme inhibitor on insulin sensitivity in fructose-fed hypertensive rats and essential hypertensives. 761 47

This study was designed to examine the effects of an angiotensin II receptor antagonist on insulin sensitivity in an insulin-resistant hypertensive rat model (fructose-fed rats; FFR). Male Sprague-Dawley rats were fed a fructose-rich diet or standard chow for 4 weeks and then treated with either 1 mg/kg/day of TCV-116 (angiotensin II receptor antagonist) or vehicle for a further 2 weeks. Steady-state plasma glucose (SSPG) was measured while the animals were conscious. Insulin (2.5 mU/kg/min) and glucose (8 mg/kg/min) were simultaneously infused to determine insulin sensitivity in each group. The mean arterial pressure (MAP) was higher in the FFR (133 +/- 5 mmHg) than in the control group (120 +/- 3), and TCV-116 (110 +/- 4) decreased MAP significantly. SSPG was also higher in the FFR group (207 +/- 6 mg/dl) than in the control (137 +/- 10, p < 0.01), and TCV-116 (171 +/- 7) significantly reduced SSPG. The FFR group also had higher steady-state plasma insulin (SSPI) levels than the control (107 +/- 10 microU/ml for FFR and 63 +/- 12 for control, p < 0.05), and TCV-116 attenuated the increase in SSPI (73 +/- 11, p < 0.05). Thus, the angiotensin II receptor antagonist improved insulin resistance, as assessed by determining SSPG in FFR, suggesting that angiotensin II antagonism may play an important role in improving of insulin resistance in FFR.
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PMID:Effects of an angiotensin II receptor antagonist, TCV-116, on insulin sensitivity in fructose-fed rats. 788 92

12 adult cadaver wrists were dissected to identify the regions of origin of the four palmar radio-carpal ligaments. A non-dimensionalized value, called the radio-carpal ligament ratio (RLR), was defined as the width of ligament origin from the radius divided by the length of the capitate. Both values were measured directly from radiographs of the cadaver specimens. The RLRs for the four palmar radio-carpal ligaments were found to be statistically consistent. We applied the RLR concept retrospectively to 20 wrists with intraarticular distal radius fractures requiring open reduction. It was found that those fracture patterns in which the fracture fragment ratios (FFR: widths of the fracture fragments divided by the length of the capitate) were outside the limits of corresponding RLRs had clear intra-operative evidence of palmar radio-carpal ligament disruption, while those with FFRs within the limits of corresponding RLRs were noted to have no ligament disruption.
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PMID:Predicting palmar radio-carpal ligament disruption in fractures of the distal articular surface of the radius involving the palmar cortex. 816 64

Factor VIIIa, the cofactor for the factor IXa-dependent conversion of factor X to factor Xa, is proteolytically inactivated by activated protein C (APC). APC cleaves at two sites in factor VIIIa, Arg336, near the C terminus of the A1 subunit; and Arg562, bisecting the A2 subunit (Fay, P., Smudzin, T., and Walker, F. (1991) J. Biol. Chem. 266, 20139-20145). Factor VIIIa increased the fluorescence anisotropy of fluorescein-Phe-Phe-Arg factor IXa (Fl-FFR-FIXa; Kd = 42.4 nM), whereas cleavage of factor VIIIa by APC eliminated this property. Isolation of the APC-cleaved A1/A3-C1-C2 dimer (A1336/A3-C1-C2), and the fragments derived from cleaved A2 subunit (A2N/A2C), permitted dissection of the roles of individual cleavages in cofactor inactivation. Intact A1/A3-C1-C2 dimer increased Fl-FFR-FIXa anisotropy and bound factor X in a solid phase assay, while these activities were absent in the A1336/A3-C1-C2. However, the residues removed by this cleavage, Met337 Arg372, did not directly participate in these functions since neither a synthetic peptide to this sequence nor an anti-peptide polyclonal antibody blocked these activities using intact dimer. CD spectral analysis of the intact and truncated dimers indicated reduced alpha and/or beta content in the latter. The A1/A3-C1-C2 dimer plus A2 subunit reconstitutes cofactor activity and produced a factor VIIIa-like effect on the anisotropy of Fl-FFR-FIXa. However, when A2 was replaced by the A2N/A2C fragments, the resulting fluorescence signal was equivalent to that observed with the dimer alone. These results indicate that APC inactivates the cofactor at two levels within the intrinsic factor Xase complex. Cleavage of either subunit modulates the factor IXa active site, suggesting an essential synergy of interactive sites in factor VIIIa. Furthermore, cleavage of the A1 site alters the conformation of a factor X binding site within that subunit, thereby reducing the affinity of cofactor for substrate.
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PMID:Activated protein C-catalyzed proteolysis of factor VIIIa alters its interactions within factor Xase. 862 29

To study the possible effects of Furosemide at the lung level, two groups of isolated rabbit lung preparation were studied. An experimental group underwent a pulmonary hydrostatic oedema when the pressure of the left auricle (PAI) was increased from 0.45 +/- 0.74 t0 11.8 +/- 2.9 cm of H2O, with that increase in PAI we obtained an increase of 0.457 +/- 0.51 g/min in FFR (Fluid Filtration Rate), during this stable and sustained oedema, a 2 mg/Kg dosis of Furosemide was injected every 10 minutes and the possible changes in PAP, PAI, PVA, TFL, PaO2, PaCO2 and pH was observed, but no changes were observed in these parameters during the Furosemide infusion, and the same effect was observed in the control group were the preparations were maintained in basal conditions and without oedema. These results suggests that the Furosemide hat not a direct cardio-pulmonary effects, and the only possible effects could be by increasing diuresis at renal level.
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PMID:[Effect of the administration of furosemide on the fluid filtration rate and in pulmonary artery pressure in isolated lungs of rabbits]. 873 Dec 93


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