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1.
F S Apple M A Rogers D C Casal L Lewis J L Ivy J W Lampe 《European journal of applied physiology and occupational physiology》1987,56(1):49-52
Total creatine kinase (CK) and CK MB activities were determined in gastrocnemius muscle and serum obtained from 14 female marathon runners. The level of CK MB in muscle increased significantly (p less than 0.05) after chronic exercise training from 5.3% to 10.5% of the total CK activity, but not after acute exercise (post-marathon 8.9%). No significant differences in total CK activities were detected. However, the total CK activity in the muscles were significantly (p less than 0.05) less than those previously reported from the muscle of men runners (1800 U/g, 3000 U/g respectively). No significant correlation existed between fiber type and muscle CK MB activity. Additionally, trace amounts of mitochondrial CK and CK BB were present in muscle homogenates. A significant correlation was observed in the increase in mean serum total CK (597 UL-1) and CK MB (23 UL-1) activities 24 h after the race (r = 0.97, p less than 0.05). These results suggest that gastrocnemius muscle in women adapts to training with increased CK MB activities and imply that skeletal muscle is the major source of elevated serum CK MB activities in women marathon runners. 相似文献
2.
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4.
P J van den Broek A S Lampe G A Berbée J Thompson R P Mouton 《BMJ (Clinical research ed.)》1985,291(6500):949-950
In an epidemic of prosthetic valve endocarditis caused by Staphylococcus epidermidis the surgeon was found to be the source of contamination. The probable route was accidental puncture of gloves during operation. During the epidemiological investigation a second cluster of patients contaminated with Staph epidermidis during open heart surgery was found also related to one surgeon. This strain caused no detectable signs or symptoms of infection. Carriage of virulent staph epidermidis has rarely been recognised as a hazard but may have serious consequences. 相似文献
5.
Electron microscopy and hydrodynamic properties of blood clotting factor V and activation fragments of factor V with phospholipid vesicles 总被引:3,自引:0,他引:3
P D Lampe M L Pusey G J Wei G L Nelsestuen 《The Journal of biological chemistry》1984,259(15):9959-9964
The electron microscopic and hydrodynamic properties of factor V and factor Va-vesicle complexes were determined. Images of negatively stained factor V bound to vesicles showed the protein as a relatively large globular domain (9.5 nm diameter) connected to the membrane through a narrow protein region 0.5-3 nm in length. This connecting region was not always visible and was measured as the distance between the globular region and the apparent vesicle edge. Factor V protein alone usually appeared as two connected globular regions of 10.2 and 6.5 nm diameter. The two-domain protein structure appeared consistent with both the image of factor V alone and bound to the membrane. Factor V had no biological activity in a phospholipid-free prothrombinase assay system used. The proteolytically activated form of factor V generated by digestion with thrombin (factor Va) was at least 30,000 times more active. The electron microscopic images of factor Va-vesicle complexes showed a smaller protein that was more closely associated with the vesicle surface than was factor V. The light chain (Mr about 80,000) component of factor Va also bound to the surface of the vesicles and appeared to be largely external to the membrane. Protein-induced hydrodynamic radius changes for the factor V-vesicle and factor Va-vesicle complexes were 12.8 and 6.3 nm, respectively. The images observed in the electron microscope were used to calculate protein-induced radius changes. Comparison of these values with the experimentally determined hydrodynamic radius changes showed approximate agreement for factor Va-membrane complexes. However, the images of factor V-vesicle complexes suggested smaller hydrodynamic radius changes than were actually observed. 相似文献
6.
A method of diagnosing the sulphur nutrition status of herbage 总被引:3,自引:2,他引:1
7.
M A Tavianini P J Gkonos T H Lampe B A Roos 《Molecular endocrinology (Baltimore, Md.)》1989,3(4):605-610
The hypothalamic peptide hormone TRH is also found in other tissues, including the thyroid. While TRH may be regulated by T3 in the hypothalamus, other regulators of TRH have not been identified and the regulation of TRH in nonhypothalamic tissues is unknown. We recently demonstrated the biosynthesis of TRH in the CA77 neoplastic thyroidal C cell line. We studied the regulation of TRH by dexamethasone in this cell line because glucocorticoids have been postulated to inhibit TSH secretion by decreasing TRH in the hypothalamus. Furthermore, TRH in the thyroid inhibits thyroid hormone release. Thus by regulating thyroidal TRH, glucocorticoids could also directly affect thyroid hormone secretion. Treatment of CA77 cells for 4 days with dexamethasone produced dose-dependent increases in both TRH mRNA and cellular and secreted TRH. Increases in TRH mRNA and peptide levels could be seen with 10(-9) M dexamethasone. A 4.8-fold increase in TRH mRNA and a 4-fold increase in secreted peptide were seen with 10(-7) M dexamethasone. Dexamethasone treatment did not increase beta-actin mRNA levels or cell growth. These results suggest that glucocorticoids may be physiological regulators of TRH in normal C cells. In addition to their inhibitory effects on TSH, glucocorticoids may decrease thyroid hormone levels by increasing thyroidal TRH. Since the glucocorticoid effects on C cell TRH are the converse of what is expected for hypothalamic TRH, glucocorticoid effects in these two tissues may be mediated by different regulators. 相似文献
8.
E. Modesto P. D. Lampe M. C. Ribeiro D. C. Spray A. C. Campos de Carvalho 《The Journal of membrane biology》1996,154(3):239-249
Membrane fractions highly enriched in chicken lens MIP (MIP28) were found to form ion channels when incorporated into planar
lipid bilayers. The channels displayed prominent unitary conductances of about 60 and 290 pS in symmetric 150 mm KCl solution and were slightly anion selective. For both depolarizing and hyperpolarizing voltages, voltage sensitivity of
the MIP28-induced conductance could be fit by a Boltzmann relation, symmetric around zero mV, with V
0
= 18.5 mV, n= 4.5 and g
min/g
max= 0.17. Channel properties were not appreciably altered by pH in the range of 5.8 to 7, although channel incorporation was
observed to occur more frequently at lower pH values. Calcium, at millimolar concentrations, decreased the channel mean open
time. Partial proteolysis of MIP28 to yield MIP21 did not appreciably affect single-channel conductance or voltage sensitivity
of the reconstituted channels. MIP28 was not phosphorylated by cAMP dependent protein kinase (PKA). Although unitary conductance
and selectivity of the chicken MIP channel are similar to those reported for the bovine MIP (MIP26), the voltage sensitivity
of MIP28 was higher than that of the bovine homologue, and voltage sensitivity of MIP28 was not modulated by treatments previously
shown to affect MIP26 voltage gating (partial proteolysis and protein phosphorylation by PKA: (Ehring et al., 1990). The existence
of such strikingly different functional properties in highly homologous channel isoforms may provide a useful system for exploration
of the structure-function relations of MIP channels.
Received: 27 March 1996/Revised: 5 August 1996 相似文献
9.
Patricia A. Lampe Ellen B. Cornbrooks Anna Juhasz Eugene M. Johnson James L. Franklin 《Developmental neurobiology》1995,26(2):205-212
Rat sympathetic neurons undergo programmed cell death (PCD) in vitro and in vivo when they are deprived of nerve growth factor (NGF). Chronic depolarization of these neurons in cell culture with elevated concentrations of extracellular potassium ([K+]o) prevents this death. The effect of prolonged depolarization on neuronal survival is thought to be mediated by a rise of intracellular calcium concentration ([Ca2+]i) caused by Ca2+ influx through voltage-gated channels. In this report we investigate the effects of chronic treatment of rat sympathetic neurons with thapsigargin, an inhibitor of intracellular Ca2+ sequestration. In medium containing a normal concentration of extracellular Ca2+ ([Ca2+]o), thapsigargin caused a sustained rise of intracellular Ca2+ concentration and partially blocked death of NGF-deprived cells. Elevating [Ca2+]o in the presence of thapsigargin further increased [Ca2+]i, suggesting that the sustained rise of [Ca2+]i was caused by a thapsigargin-induced Ca2+ influx. This treatment potentiated the effect of thapsigargin on survival. The dihydropyridine Ca2+ channel antagonist, nifedipine, blocked both a sustained elevation of [Ca2+]i and enhanced survival caused by depolarization with elevated [K+]o, suggesting that these effects are mediated by Ca2+ influx through L-type channels. Nifedipine did not block the sustained rise of [Ca2+]i or enhanced survival caused by thapsigargin treatment, indicating that these effects were not mediated by influx of Ca2+ through L-type channels. These results provide additional evidence that increased [Ca2+]i can suppress neuronal PCD and identify a novel method for chronically raising neuronal [Ca2+]i for investigation of this and other Ca2+-dependent phenomena. © 1995 John Wiley & Sons, Inc. 相似文献
10.
We have isolated an eight kilobase fragment of Bacillus subtilis DNA by specific integration and excision of a plasmid containing a sequence adjacent to ribosomal operon rrn O. The genetic locus of the cloned fragment was verified by linkage of the integrated vector to nearby genetic markers using both transduction and transformation. Functional gyrA activity encoded by this fragment complements E. coli gyrA mutants. Recombination between the Bacillus sequences and the E. coli chromosome did not occur. The Bacillus wild type gyrA gene, which confers sensitivity to nalidixic acid, is dominant in E. coli as is the E. coli gene. The cloned DNA precisely defines the physical location of the gyrA mutation on the B. subtilis chromosome. Since an analogous fragment from a nalidixic acid resistant strain has also been isolated, and shown to transform B. subtilis to nalidixic acid resistance, both alleles have been cloned. 相似文献