Contraction kinetics of striated muscle fibres following quick changes in load

1. The contraction kinetics of single striated muscle fibres and small fibre bundles from the frog and the toad were measured when the load was changed from P(0) to L < P(0). Simultaneous recordings were made of displacement at one end and force at the other end of the preparation.2. After the load was changed, the contractile force generally reached a steady value before the contraction velocity became steady. The amount of time required for isotonic contraction to become steady depended on the change in fractional load and on the temperature; it did not depend on sarcomere length in the range 2.2-3.0 mu or on the number of fibres in the preparation. The characteristics of the non-steady state are described in terms of the displacement deviation (the difference between the actual displacement at a given time and the back extrapolation of the steady phase of the displacement record) and the null times (the times at which the displacement deviation became zero, measured relative to the time at which the contractile force first reached the value of the load).3. The time average of the transient velocity was approximately equal to the final steady velocity.4. The product of the null time following a given relative force step and V(max), the steady velocity of unloaded contraction, was found to be independent of temperature. This is taken as evidence that the isotonic velocity transients originate in the contractile mechanism.5. The non-steady state following step changes in load is identified with the motion of cyclic contraction mechanisms. The motion of the specific model formulated by A. F. Huxley (1957) was compared with that of frog muscle fibres and, although the transients in the two systems differ in detail, the characteristic dimensions are of the same order.     

Evaluation of Suspected Monoclonal Gammopathies: Experience in a Tertiary Care Hospital

Background

Monoclonal gammopathies occurs in patients with malignant diseases of plasma cells and lymphocytes and in few benign conditions. The objective of this study was to assess the precision, accuracy and confirmation of monoclonal gammopathies on serum protein electrophoresis (SPE) and the clinical relevance of detection and characterization of M component.

Methods

All samples received for serum electrophoresis in the last 3 years were analysed for data on M band positivity and correlating it with clinical profile of the patients. Immunofixation (IFE), Immunoelectrophoresis (IEP) and IgG, IgM estimation were carried out in few cases. The follow up of cases was done by serial monitoring of SPE and β₂ microglobulin levels.

Results

1155 samples were received during the 3 years period. 282 (24.4%) samples were positive for M component on SPE. Of these, 239 (84.8%) patients had M spike in λ region and 43 patients had M spike in β region. The mean load of the M protein band in the λ region was 37.8% and in β region was 35.8%. IgG with κ chain was seen in 40%, IgG with λ chain was seen in 50%, 5% patients each had IgM with κ and IgA with λ light chain. 246 samples (96.5%) had high levels of β₂ microglobulin. Of the 116 cases of multiple myeloma, IgG levels was more commonly raised (5%) as compared to IgA (6.9%) and IgM (5.2%).

Conclusion

It is recommended that SPE should be performed in patients having unexplained weakness, anaemia, back pain, osteoporosis, osteolytic lesions, fractures, renal insufficiency or recurrent infections.Key Words: Serum protein, Electrophoresis, M band, Multiple myeloma     

Absence of sleep-related growth hormone elevations in myotonic dystrophy

There is evidence that in myotonic dystrophy, the endocrine and central nervous systems are affected. To study a possible relationship between both defects, we investigated nocturnal sleep patterns and associated growth hormone secretion in two men and three women with myotonic dystrophy. In three patients who were clinically the most severely affected by myotonic dystrophy, plasma growth hormone elevations related to the slow-wave phase of sleep were absent. The two least severely affected patients had plasma growth hormone increases of low magnitude and brief duration (from 0.4 ng per milliliter to 13.0 ng per milliliter). These data suggest a failure of integration at a subcortical level of the slow-wave phase of sleep with the hypothalamic-pituitary mechanisms of growth hormone secretion. Thalamic neuronal lesions occurring in myotonic dystrophy could be responsible for such failure.