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Intracellular calcium during fatigue of cane toad skeletal muscle in the absence of glucose (2000)

Kabbara, A. A. ; Nguyen, L. T. ; Stephenson, G. M. M. ; [et al.]

Springer

Journal of muscle research and cell motility 21 (2000), S. 481-489

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ISSN: 1573-2657

Source: Springer Online Journal Archives 1860-2000

Topics: Biology , Medicine

Notes: Abstract Mechanisms of fatigue were studied in single muscle fibres of the cane toad (Bufo marinus) in which force, intracellular calcium ([Ca2+]i), [Mg2+]i, glycogen and the rapidly releasable Ca2+ from the sarcoplasmic reticulum (SR) were measured. Fatigue was produced by repeated tetani continued until force had fallen to 50%. Two patterns of fatigue in the absence of glucose were studied. In the first fatigue run force fell to 50% in 8–10 min. Fatigue runs were then repeated until force fell to 50% in 〈3 min in the final fatigue run. Addition of extracellular glucose after the final fatigue run prolonged a subsequent fatigue run. In the first fatigue run peak tetanic [Ca2+]i initially increased and then declined and at the time when force had fallen to 50% tetanic [Ca2+]i was 54 ± 5% of initial value. In the final fatigue run force and peak tetanic [Ca2+]i declined more rapidly but to the same level as in first fatigue runs. At the end of the first fatigue run, the rapidly releasable SR Ca2+ store fell to 46 ± 6% of the pre-fatigue value. At the end of the final fatigue run the rapidly releasable SR Ca2+ store was 109 ± 16% of the pre-fatigue value. In unstimulated fibres the nonwashable glycogen content was 176 ± 30 mmol glycosyl units/l fibre. After one fatigue run the glycogen content was 117 ± 17 mmol glycosyl units/l fibre; at the end of the final fatigue run the glycogen content was reduced to 85 ± 9 mmol glycosyl units/l fibre. [Mg2+]i did not change significantly at the end of fatigue in either the first or the final fatigue run suggesting that globally-averaged ATP does not decline substantially in either pattern of fatigue. These results suggest that different mechanisms are involved in the decline of tetanic [Ca2+]i in first compared to final fatigue runs. The SR Ca2+ store is reduced in first fatigue runs; this is not the case for the final fatigue run which is associated with a decline in glycogen and possibly related to either a non-metabolic effect of glycogen or a spatially-localised metabolic decline.

Type of Medium: Electronic Resource

URL: http://dx.doi.org/10.1023/A:1005650425513

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Glycogen stability and glycogen phosphorylase activities in isolated skeletal muscles from rat and toad (2000)

Goodman, Craig A. ; Stephenson, Gabriela M. M.

Springer

Journal of muscle research and cell motility 21 (2000), S. 655-662

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ISSN: 1573-2657

Source: Springer Online Journal Archives 1860-2000

Topics: Biology , Medicine

Notes: Abstract There is increasing evidence that endogenous glycogen depletion may affect excitation–contraction (E–C) coupling events in vertebrate skeletal muscle. One approach employed in physiological investigations of E–C coupling involves the use of mechanically skinned, single fibre preparations obtained from tissues stored under paraffin oil, at room temperature (RT: 20–24°C) and 4°C for several hours. In the present study, we examined the effect of these storage conditions on the glycogen content in three muscles frequently used in research on E–C coupling: rat extensor digitorum longus (EDL) and soleus (SOL) and toad iliofibularis (IF). Glycogen content was determined fluorometrically in homogenates prepared from whole muscles, stored under paraffin oil for up to 6 h at RT or 4°C. Control muscles and muscles stored for 0.5 and 6 h were also analysed for total phosphorylase (Phostotal) and phosphorylase a (Phos a) activities. No significant change was observed in the glycogen content of EDL and SOL muscles stored at RT for 0.5 h. In rat muscles stored at RT for longer than 0.5 h, the glycogen content decreased to 67.6% (EDL) and 78.7% (SOL) of controls after 3 h and 25.3% (EDL) and 37.4% (SOL) after 6 h. Rat muscles stored at 4°C retained 79.0% (EDL) and 92.5% (SOL) of glycogen after 3 h and 75.2% (EDL) and 61.1% (SOL) after 6 h. The glycogen content of IF muscles stored at RT or 4°C for 6 h was not significantly different from controls. Phostotal was unchanged in all muscles over the 6 h period, at both temperatures. Phos a was also unchanged in the toad IF muscles, but in rat muscles it decreased rapidly, particularly in EDL (4.1-fold after 0.5 h at RT). Taken together these results indicate that storage under paraffin oil for up to 6 h at RT or 4°C is accompanied by minimal glycogen loss in toad IF muscles and by a time- and temperature-dependent glycogen loss in EDL and SOL muscles of the rat.

Type of Medium: Electronic Resource

URL: http://dx.doi.org/10.1023/A:1005628500892

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Assessing the conditions forin vivo electrical virtual biopsies in Barrett's oesophagus (2000)

González-Correa, C. A. ; Brown, B. H. ; Smallwood, R. H. ; [et al.]

Springer

Medical & biological engineering & computing 38 (2000), S. 373-376

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ISSN: 1741-0444

Keywords: Virtual biopsies ; Barrett's oesophagus ; Bio-electrical impedance

Source: Springer Online Journal Archives 1860-2000

Topics: Biology , Chemistry and Pharmacology , Medicine

Notes: Abstract It has previously been shown that it is possible to differentiate between squamous and columnar epithelia in rat and resected human tissues using an impedance probe to makein vitro measurements. This probe can be passed down an endoscope allowing measurements to be made in patients. However, the probe emerges parallel to the oesophageal wall, with little room to manoeuvre. The conditions of control required to give reliable readings have been investigated. The importance of pressure applied and the angle of approach to the oesophagus was assessed. Pressures in the range 26.6 Pa to 46.3 kPa and angles in the range 15–90 degrees were considered. Inin vitro studies it was observed that it was possible to obtain consistent readings with pressures greater than 2.9 kPa and with angles greater than 15 degrees between the probe and the oesophagus. These conditions can be achievedin vivo, and readings obtained from twelve patients are shown (45 readings on normal squamous, 34 on Barrett's oesophagus and 22 on stomach). At low frequencies (9.6–153.2 kHz), a Mann-Whitney test shows a significant difference (p〈0.001) when comparing the means from squamous and columnar, and also when readings from Barrett's and normal gastric epithelia are compared (p〈0.001).

Type of Medium: Electronic Resource

URL: http://dx.doi.org/10.1007/BF02345004

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Co-segregation of elevated LDL with a novel mutation (D92K) of the LDL receptor in a kindred with multiple lipoprotein abnormalities (2000)

Wu, L. L. ; Hopkins, P. N. ; Xin, Y. ; [et al.]

Springer

Journal of human genetics 45 (2000), S. 154-158

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ISSN: 1435-232X

Keywords: Key words Hyperlipoproteinemia ; Lipoproteins ; LDL receptor ; Familial combined hyperlipidemia

Source: Springer Online Journal Archives 1860-2000

Topics: Biology , Medicine

Notes: Abstract Factors predisposing to the phenotypic features of familial combined hyperlipidemia have not been clearly defined. In the course of investigating familial coronary artery disease in Utah, we identified a three-generation family in which multiple members were affected with type IIa hyperlipoproteinemia (HLP IIa), type IIb hyperlipoproteinemia (HLP IIb), or type IV hyperlipoproteinemia (HLP IV). Because several family members had relatively severe low-density lipoprotein (LDL) cholesterol elevation, in order to dissect the possible contribution to the plasma lipoprotein abnormalities in this pedigree, we identified a novel point mutation in the low-density lipoprotein receptor (LDLR) gene, a G-to-A transition at nucleotide position 337 in exon 4. This change substituted lysine for glutamic acid at codon 92 (D92K) of the LDL receptor. By means of mutant allele-specific amplification we determined that the mutation co-segregated with elevated cholesterol and LDL cholesterol in the plasma of family members with HLP IIa and HLP IIb, but not with the elevated plasma triglycerides seen in HLP IIb and HLP IV patients. Thus, in families with apparent familial combined hyperlipidemia, a defective LDLR allele and other genetic or environmental factors that elevate plasma triglycerides may account for the multiple lipid phenotypes observed in this kindred.

Type of Medium: Electronic Resource

URL: http://dx.doi.org/10.1007/s100380050202

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